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Remove the cleaning tape. Page Operation References Operation References Part Names For details on the use of each part, refer to the page number indicated in parentheses.

Front view Operation button p. Call your local authorized Sharp dealer to have it replaced. The battery is almost depleted when the camcorder transfers data through the USB cable. Use the AC adapter or fully charged Page 17 Displayed for Description of warning 5 seconds The card is not inserted or is inserted improperly.

Check that it is properly inserted see page Push the battery pack in the direction of the arrow until it clicks. Page 19 Slide the battery release in the pack while pressing the release. Use of other batteries may create a risk of fire or explosion. Other types of battery packs may burst, causing personal injury and damage. Close the compartment door Removing a Cassette by pressing its centre until it clicks into place.

Inserting Attach the power source to the camcorder, then slide and hold the cassette compartment door release as you open the cassette compart- ment door. Then pull the card straight out 2 as shown below. Page Installing The Lithium Batteries Preparation Installing the Lithium Insert the smaller lithium battery into the compartment with the H side of Batteries the battery facing out.

Installing the Memory Battery CR type The supplied CR type lithium battery is lithium battery used to store the memory of the date and time settings. For The CR type lithium battery camcorder, replace only with same or supplied with VL-Z5 is used to power the equivalent type CR, for remote remote control unit. Attach the strap of the lens cap to the hand strap as shown below. Open the hand strap flap 1 and grip strap 2.

You can also watch Before using a commercially available playback through the viewfinder. Viewfinder Power switch Pull out the viewfinder completely. Page Adjusting The Dioptre Preparation Closing the viewfinder Adjusting the dioptre Adjust the dioptre according to your Push in the viewfinder completely. Pull out the viewfinder completely.

Hold down the Lock button and set the Power switch to v. You can use the LCD monitor to play back recordings that you have made or to watch the subject during recording. Page Tips On Recording Positions Preparation Tips on Recording Positions To create images that are easy to watch during playback, try to record with an upright posture and steady hands to prevent a shaky image. Holding the camcorder Put your right hand through the hand strap, and place your left hand under the camcorder for support.

Page Basic Operations Basic Operations Camera Recording Selecting the Camcorder Mode Media Selection switch This camcorder includes functions for use as both a video camera for recording and playing back images on tapes and as a digital still camera for recording and playing back still images on cards. One of the following camcorder modes needs to be set before starting any operation.

Zooming allows you to move visually closer to or farther from a subject without physi- P A U S E cally changing your position. Tape Camera — When Power Standby mode, for example, is cancelled after 3 minutes, the Power Standby mode allows you to prevent camcorder will turn off if recording is not You can monitor the sound via stereo earphones commercially available during Set the Media Selection switch to V, playback or recording.

Picture noise or malfunction may occur Available modes: if any of the above is left on while Tape Playback, Card Playback making a connection. Set to the desired camcorder mode by using the Media Selection switch and the Power switch see page Use the menu screens to adjust the various Example camcorder settings. Tape Camera, Card Camera When the subject is backlit, the image will appear dark if it is recorded normally. Normal self recording Set the Power switch to v.

If left on, the recorded The windbreak function allows you to audio may sound somewhat muffled when reduce annoying noise from strong winds played back. Playback, playback will stop. In such situations, set the camcorder to Manual Focus mode and focus manually. White paper or white cloth Available modes: Tape Camera, Card Camera The colour of the subject on the screen looks different depending on lighting conditions.

Tape Playback Audio 1: Stereo left and right sound Audio 2: No audio You can add narration to recordings made with this camcorder, while preserving the bit audio recording original audio and video recordings.

Press m again Source to resume recording. Antigenic shift variants, whether resulting from whole-virus interspecies transmission or gene reassortment, can completely evade the pre-existing immunity in the host population. Antigenic shift. There are two ways that an influenza virus with new antigenic properties may enter the pig population. A Virus that was previously adapted to another animal host, such as avian species, enters pigs and adapts to circulate efficiently in swine.

The diagram portrays the inter-species transmission of an avian H1N1 virus, which became established in European swine populations; B Virus previously adapted to another host, such as birds or humans, co-infects a pig along with a common swine-adapted strain. The diagram portrays reassortment between human seasonal H1N1 and swine H3N2 viruses.

In both A and Bthe swine population lacks antibodies to important surface proteins of the new virus. The influenza A virus polymerase is error-prone, facilitating such mutations. Antigenic drift also allows the virus to evade pre-existing immune responses, although this occurs more slowly than with antigenic shifts.

Antigenic drift. A swine herd with population immunity to IAV-S has neutralizing antibodies specific to a strain that was previously encountered through infection or vaccination.

However, if antigenic drift produces a new variant strain that pre-existing antibodies in the herd are unable to neutralize, the pigs become susceptible to reinfection. Nevertheless, there is some variability, which is thought to contribute to the adaptation of the virus to a host species [ 26 ]. It entered swine populations inconcurrently with the highly virulent H1N1 Spanish flu epidemic in people [ 9111239 ].

During the human pandemic, the H1N1 human influenza virus was transmitted between people and pigs; outbreaks in farm families were often followed immediately by outbreaks in their swine herds, and outbreaks in pigs were sometimes followed by illness among humans on the farm [ 3 ]. While some authors suggest that the classical H1N1 virus might have entered swine populations from humans, the origins of this virus and direction of transfer are still unclear.

The virus circulated in both humans and pigs after this time, but diverged significantly in the two host populations [ 4142 ]. H1N1 viruses in people continued to change through antigenic drift. In contrast, classical H1N1 virus remained antigenically stable while it circulated in swine populations in North America [ 39 ]. Although some human H3 viruses were also found at low levels in pigs, no virus became established as a stable lineage during this time [ 39 ].

Triple reassortant H3N2 viruses were first detected in U. They appeared first mainly in the Midwest [ 12434445 ], and they have been detected in Canada since [ 464748 ]. This particular combination of internal genes is known as the triple reassortant internal gene TRIG cassette. The TRIG cassette seems to be particularly efficient in generating viruses with new HA and NA gene segments, and viruses carrying this cassette have reassorted with additional human influenza viruses, as well as with other influenza viruses in swine [ 394950 ].

The H3 viruses arose from at least three separate introductions of H3 human influenza viruses into pigs [ 39 ]. The N1 or N2 of these viruses is also of human lineage.

There are now four phylogenetic clusters of H1 viruses—alpha, beta, gamma and delta—endemic among pigs in the Cross My Mind - Various - FreeLuv001 (File). One of these N was introduced from human seasonal H3N2 during the original triple-reassortment event of the late s.

The other N was acquired from a human seasonal H3N2 virus that circulated around — Many herds were also infected with the pandemic H1N1 virus circulating among people. This virus entered human populations inand spread throughout the world. The pandemic H1N1 virus has been introduced repeatedly into swine herds throughout the world [ 1340575859 ]. This virus has undergone reassortment with IAV-S in the US, Canada, and other locations around the world [ 1340545859606162 ].

Other variants of the dominant subtypes are also reported periodically among pigs e. H2N3 viruses were isolated from pigs on two farms in the central U. The H2 and N3 in these viruses were from avian influenza viruses in waterfowl possibly different bird speciesand the PA was also of avian lineage, but they contained the other genes from the TRIG cassette [ 6364 ].

This virus did not seem to affect other herds [ 64 ]. However, its H2 bound well to mammalian receptors, and it might be able to replicate readily in mammals [ 39 ].

H3N1 viruses have also been found [ 6566 ], but were composed of swine-lineage H3 and N1 and thus, less of a risk to immune pig populations than truly novel subtypes such as the H2N3. With the globalization of world economies, there is a risk of introducing influenza viruses from other regions into the U. Despite the superficial similarity in subtypes, many of these viruses are different from the viruses found in North America. For example, an H1N1 virus, which has all gene segments of avian origin, has circulated among swine in Europe since the s [ 40 ].

Pandemic H1N1 has infected swine herds throughout the world, and in some cases, this virus has undergone reassortment with local IAV-S strains [ 1340 ].

The prevalence of IAV-S subtypes and lineages in African countries is also not well characterized [ 70 ]. Immunity to viruses is a complex process involving both nonspecific innate protective responses, and specific adaptive humoral and cell-mediated immunity directed against the specific virus. The various cells and soluble mediators of the immune system interact in many ways to eliminate the pathogen.

The lungs present a particular challenge for immune responses, as viruses must be eliminated, but severe inflammation must also be avoided to minimize tissue damage. Innate responses include chemical, physical and cellular responses that are immediately protective against a broad range of invading microorganisms. Type I interferons, in turn, have a number of antiviral properties that inhibit influenza virus replication [ 39 ]. Conversely, the influenza A virus protein NS1 can inhibit interferon-mediated host defenses [ 24252672 ].

Other components of innate responses, including macrophages [ 73 ] and natural killer NK cells [ 74 ] also play roles during influenza A virus infections. Innate immune responses contribute to the activation of adaptive immunity [ 72 ].

Adaptive immune responses are traditionally divided into humoral immunity, which includes those mechanisms that are dependent on antibodies, and cell-mediated immunity CMIin which immune cells cytotoxic T cells directly recognize and destroy infected host cells.

Antibody responses can be induced by any protein that enters the body, including those of killed viruses e. Cytotoxic T cell responses are induced optimally by live organisms such as IAV replicating inside cells. The critical immune cell types for both humoral immunity and CMI are various types of lymphocytes B or T lymphocytes. Each lymphocyte responds very specifically to the immunogenic portions of that virus, called antigens.

Most antigens are proteins. In reality, each lymphocyte actually responds to a tiny piece of the viral protein, called an epitope.

Epitopes may be shared between strains of influenza viruses, or may be unique to a strain. Depending on the epitopes that are recognized, immune responses may be more or less broadly protective against different viral strains. Some subpopulations of responding lymphocytes also differentiate into memory cells, which respond more strongly when they encounter the same virus a second time. Antibodies are important in preventing influenza virus infections and in reducing the severity of disease [ 39 ].

Antibodies are made by B cells also called B lymphocytes. B cells can make different isotypes of antibodies. Antibody isotypes differ in their ability to carry out the various humoral immune responses that defend the body from pathogens.

Helper T cells are critical for the production of high quality IgG and IgA antibodies that have high affinity to the antigen. Antibodies to the HA of IAV-S can be found in the respiratory tract of pigs as soon as 4—5 days after infection with IAV-S [ 7576 ], and serum titers appear in approximately 7 days [ 777879 ], although peak levels occur later e.

Both local IgA and IgG are found in the respiratory tract of influenza virus-infected pigs [ 397576788081 ]. Protective antibody responses in the lungs are often, but not always, correlated with the serum antibody titers in the blood [ 398283 ]. In laboratory animals such as mice, memory B cells specific for influenza A viruses can be found for many months in the respiratory tract and other tissues [ 71 ].

Humans can develop long-term antibody responses to some antigens, possibly spanning many decades [ 71 ]. The influenza A virus HA usually induces the strongest antibody responses after infection [ 84 ], probably because this protein is present in large amounts on the surface of the virus.

Antibody titers to the HA are, however, affected by the dose of virus [ 71 ], and possibly its subtype. In some studies, pigs infected with H3N2 viruses had higher serum antibody titers than pigs infected with H1N1 or H1N2 viruses [ 337985 ]. Some antibodies to the HA, called neutralizing antibodies, can block this protein from attaching to its sialic acid receptor, and thus prevent the virus from infecting cells.

Well-matched antibodies to the HA can be sufficient to prevent an influenza virus infection, and also contribute to clearing the virus from the lungs [ 7186 ]. Whether the antibody response to the HA can protect the animal from a different viral strain depends on the similarity between the HA proteins of the two viruses [ 72 ].

This is influenced not only by the overall genetic similarity between these proteins, but on how well the individual epitopes match; changes in some parts of the HA can influence protection more than others [ 87 ]. Neutralizing antibody responses are thought to be the most important immune responses for protecting pigs against closely related IAV-S of the same subtype [ 718083 ].

Protective immunity mediated by neutralizing antibodies can be predicted by the magnitude of serum antibody activity against the particular IAV-S strain, e. Animals exposed to influenza viruses normally make fewer antibodies to the NA than the HA [ 84 ]. Humoral responses to the NA have not been studied as extensively, but they may also be important in protection [ 2829303172 ].

Antibodies to the NA are thought to reduce the ability of the virus to spread from cell to cell, by preventing this enzyme from cleaving sialic acids [ 7286 ]. They might also prevent the NA from clearing a path through the respiratory tract mucus layer and cell glycocalyx [ 86 ].

Similarly to the HA, mutations in the NA can reduce the protective effects of pre-existing antibodies [ 72 ], although the NA has a somewhat slower mutation rate [ 909192 ]. Antibodies might also contribute to immunity against influenza viruses by alternative mechanisms. In some cases, antibodies can promote the ingestion of viruses by phagocytes cells, such as macrophages, which engulf and destroy many pathogens.

These cells have receptors that can recognize part Vanki - Kaaos - Ristiinnaulittu Kaaos (Vinyl, Album, LP) the antibody molecule, essentially tethering the virus to the cell via the antibody. The virus is then ingested and destroyed.

Similarly, some immune cells, such as macrophages, can recognize antibodies attached to viral antigens on infected cells, and destroy the infected cell. This mechanism is known as antibody-dependent cell cytotoxicity ADCC. Based on studies in mice, cell-mediated immune responses CMI are thought to be critical for complete viral clearance once the influenza virus has infected cells [ 93 ]. There is evidence that these responses also occur in the lungs of pigs infected with IAV-S [ 819495 ].

However, CMI responses do not prevent infection [ 80 ]. In humans, cell-mediated immunity to influenza was correlated with reduced virus shedding, when antibodies to the virus were absent [ 96 ]. CMI is primarily mediated by cytotoxic T cells.

These T lymphocytes play an important role in eliminating influenza virus-infected cells [ 73 ]. They recognize fragments of viral proteins epitopes displayed on the surfaces of infected cells in MHC I molecules. CMI responses are usually directed to the internal, conserved proteins of influenza viruses [ 718097 ], especially the NP [ 9899]. Cytotoxic T cells eliminate influenza Ments Meg Álmaimtól - Sass Sylvia* - Nézz Körül (Vinyl, LP, Album) cells through two major mechanisms [ ].

In one, they produce molecules called perforins, which insert themselves into the cell membrane of the infected cell and lyse it. In pigs, activated T cells have been reported as early as 5—7 days after infection with influenza viruses [ 7795 ].

Protection between less closely related influenza viruses seems to depend, in part, on CMI reactions to the conserved internal proteins of the influenza virus [ 71728087, ]. It is not practical to measure CMI outside the research laboratory setting; however, it is important to realize that some critical immune responses to the virus may take place independently of antibody titers measured in the blood.

In addition, Huora - Appendix - 82/83 (Cassette), inactivated influenza vaccines for swine stimulate limited CMI compared to natural exposure, limiting the breadth of protection they can provide.

Factors that may influence vaccine efficacy include homology between the vaccine and challenge strains, the immunogenicity of vaccine components, the quantity of antigen included, and the adjuvant used. Matching of the viral HA is a critical component in vaccination because the goal of inactivated vaccines is mainly to produce neutralizing antibodies to this protein [ 80 ].

Responses to the NA may also be protective [ 28293031 ]. While there have been reports of CMI responses to inactivated influenza vaccines in swine [ ], CMI and mucosal immune responses to these vaccines are generally thought to be very limited [ 94, ]. A poor CMI response to an inactivated vaccine limits its ability to cross-protect against strains with antigenically divergent HA and NA Light Blue - Ron Carter - All Blues (Vinyl, LP). A recent study tested an intranasal IAV-S vaccine containing inactivated virus and a synthetic adjuvant called poly I:C [ ].

Compared with a conventional inactivated vaccine, the intranasal poly I:C adjuvanted vaccine induced higher cross-reactive serum HI antibody titers and somewhat greater protection against heterologous challenge.

Newborn piglets have no maternal antibodies at birth, as these proteins cannot cross the placenta in swine [ 1 ]. Although neonatal piglets are able to mount immune responses, their immune system appears to be underdeveloped at birth, and less able to respond to pathogens and vaccines for the first few weeks [ ].

Although the gut closes to the absorption of antibodies and cells after approximately 36 hours, piglets continue to receive passive mucosal IgA antibodies in their gastrointestinal tract from the milk until weaning [ 1 ]. A common strategy to control IAV-S is to vaccinate sows, which then transfer this protection to their piglets in colostrum.

As the maternal antibodies decline, however, the piglets become susceptible to infection. In the offspring of these sows with high titers, maternal antibodies have been found to persist until 14—16 weeks, while they often disappear around 6 weeks in piglets born to exposed but unvaccinated dams [ ] cited in [ 79 ].

Although they may protect the piglet, maternal antibodies can interfere with the development of active immunity after infection or vaccination [ ]. In several studies, piglets with maternal antibodies had no rise in HI titers after they were exposed to IAV-S [, ]. Other groups reported that such piglets did respond to infection or vaccination, though more weakly.

In one study, 7-week-old piglets with low levels of maternal antibodies developed lower HI titers, virus-specific immunoglobulins, and T cell proliferative responses compared to piglets without maternal antibodies, when they were infected with the same H1N1 virus that had been used to vaccinate their dams [ ].

Nevertheless, these pigs did mount an immune response that resulted in less severe clinical signs, compared to naive pigs, when they were re-exposed to the virus at 15 weeks of age. In another study, piglets vaccinated with a bivalent inactivated vaccine at 1 and 4 weeks, 1 and 8 weeks, 4 and 8 weeks, 8 and 10 weeks, or 8 and 12 weeks of age had detectable HI titers after the second dose [ ]. The titers were lower in piglets with passive maternal antibodies.

Other studies have shown that it is possible for piglets to develop cell-mediated immune responses CMI to antigens despite the presence of maternal antibodies [ ]. Results of another study suggest that inactivated IAV-S can induce greater HI antibody titers and cross-protection in maternal antibody-positive piglets if it is formulated with poly I:C adjuvant and administered intranasally [ ].

Maternal antibodies sometimes provide pigs with partial or complete protection from disease after inoculation with IAV-S [,], although protection may vary depending on the antibody titer [ ].

One of these studies examined overall growth rates, as well as clinical signs, after two exposures to the same influenza virus [ ]. In this study, 7-week-old piglets without maternal antibodies grew more slowly immediately after they were inoculated with IAV-S, compared to piglets with maternal antibodies; however, the animals in the two groups were similar in size 3 weeks later.

When both groups of piglets were exposed to this virus again at 15 weeks Im Getting Sentimental Over Yiou - Lorne Greene - Young At Heart (Vinyl, LP, Album) age, the piglets without maternal antibodies seemed to have higher growth rates overall.

The explanation appeared to be that these animals were less affected by the second exposure to the virus. Piglets protected from clinical signs by maternal antibodies may still become infected and shed virus [,]. In some experiments, piglets with low levels of maternal antibodies shed IAV-S at least as long [ ] or longer [ ] than piglets without Huora - Appendix - 82/83 (Cassette) antibodies.

In contrast, high maternal antibody titers inhibited virus shedding in one of these two studies [ ]. Neonatal piglets that become infected might act as reservoirs for influenza viruses under some field conditions even when viruses are not detected in the breeding sows []. An H1N1 virus could be detected for up to 70 days in one group of growing pigs housed in a finishing barn, when no additional animals were added to the group [ ]. Piglets with waning maternal antibodies could be infected with IAV-S from older pigs or other sources of the virus, and these viruses may be transmitted relatively slowly among the growing pigs.

A small number of animals infected at weaning might act as the source of virus for the rest of the cohort, and could also transport the virus to distant production units. Vaccination of sows might be able to decrease virus transmission in some cases.

In one study, high and uniform titers of maternal antibodies to an H1N1 virus reduced the transmission of the same virus, although it did not prevent the transmission of an H1N1 virus that belonged to a different phylogenetic cluster [ ].

Supportive evidence is also provided by a report from the field, in a herd where mass vaccination of sows was able to boost maternal antibody levels sufficiently to stop an outbreak of respiratory disease among suckling and nursery piglets [ 7 ].

Based on these studies, sow vaccination often provides piglets a measure of protection, but stopping virus transmission in the herd requires a close antigenic match between the sow vaccine and the local circulating strain s. New subtypes or strains of influenza resulting from antigenic shift or drift may produce an increased threat to animal and human health.

These emerging influenza variants can be identified by monitoring changes in circulating influenza virus strains in swine. Documents included at this website are as follows:. Influenza Surveillance in Swine Procedures Manual [ ]:. Implementation of the program formally began in The objectives of this surveillance program are to:.

Monitor genetic evolution of endemic influenza in swine to better understand endemic and emerging influenza virus ecology. Make available influenza isolates for research and to establish an objective database for genetic analysis of these isolates and related information; and.

Select proper isolates for the development of relevant diagnostic reagents, updated diagnostic assays, and vaccine seed stock products. In designing the program to meet these objectives, special care was taken to give veterinarians and producers flexibility to participate without concern that IAV-S detection would bring scrutiny to their operations.

Sharing of data and viral isolates is encouraged so that public health authorities, researchers and manufacturers will be equipped with information and materials that are as contemporary as possible. To meet both of these goals, veterinarians and producers are given the option to submit specimens anonymously. In order to optimize resources and provide a level of uniformity in sampling, the surveillance program is focused toward sampling from swine that meet specific criteria.

Case-compatible swine accessions submitted to veterinary diagnostic laboratories. This stream includes samples submitted by producers, veterinarians or other personnel who observe pigs exhibiting influenza-like illness ILI on farms.

Samples collected for routine diagnostic testing may also be tested at the laboratory for influenza as part of the surveillance program. Swine exhibiting ILI at first points of concentration or commingling events such as auctions, markets, fairs or other swine exhibition events. The veterinarian in charge or animal health official may segregate, examine and collect appropriate samples from pigs exhibiting ILI.

These samples would be submitted to a veterinary diagnostic lab and tested for IAV-S as part of the surveillance program. Swine populations epidemiologically linked to a confirmed isolation of IAV-Sin a human. The U. The surveillance information is divided into five categories including virological surveillance, outpatient illness surveillance, mortality surveillance, hospitalization surveillance and summary of the geographic spread of influenza [ ].

Occasionally, an epidemiological link may be suspected when human influenza cases have a recent history of exposure to pigs. The number of samples collected will be determined on a case-by-case basis. Samples may be collected and submitted from producers, veterinarians, animal health officials or other personnel [ ].

Animals to be sampled should be febrile if possible some IAV-S strains induce a minimal febrile response with serous nasal discharge and cough. Samples may include nasal swabs, oral fluids, and lung tissue. Up to ten samples from animals which fit the case definition may be sampled per diagnostic case under the IAV-S Surveillance Program.

Lung tissue collected from mortalities or euthanized animals may be submitted in plastic bags or screw-top plastic tubes. When collecting samples using nasal swabs, polyester or flocked swabs are inserted deep into the nasal cavity while the pig is restrained.

The swab is rotated to collect surface epithelium as well as mucosal secretions from both nostrils. Blood on the swabs may interfere with testing, so caution should be taken in rotating too vigorously or inserting the swab too deeply. Swabs should be inserted into virus transport media. Once the samples are collected, they should be chilled until shipped or shipped as soon as possible with ice packs.

The network is organized and supported so that it has the capacity to respond to animal-disease outbreaks nationwide and is the model for effective diagnostic networks, able to respond and communicate diagnostic outcomes to decision makers quickly.

NAHLN laboratories perform routine diagnostic tests for endemic animal diseases like IAV-S as well as targeted surveillance and response testing for foreign animal diseases in the event of an outbreak. Samples are tested from the following swine populations. As with any routine diagnostic work-up, NAHLN diagnostic labs conduct tests requested by the veterinarian and report test results to the submitting veterinarian as per the usual process.

IAV-S Surveillance Program test results are reported as anonymous unless the producer is willing to participate in the traceable surveillance option []. Producers participating in the traceable surveillance option receive surveillance test results.

No additional charges to the submitter result from testing conducted in accordance with either the anonymous or traceable surveillance streams of the IAV-S Surveillance Program. Data are collected by NAHLN, or through direct messaging between laboratory information management systems. Data are then monitored and analyzed by the USDA, in collaboration with industry stakeholders and the office of the State Animal Hospital - The Modern Lovers - Precise Modern Lovers Order (Live In Berkeley And Boston) (CD, Album) Official SAHOto identify sequences and data that may initiate further research or targeted surveillance.

Data confidentiality and security are priorities. When submitted through traceable surveillance, the response to unusual test results is determined on a case-by-case basis. As with the case-compatible swine accessions, unless written permission is provided by the owners of pigs sampled for traceable surveillance, test results will be entered through the anonymous surveillance stream. The SAHO determines the control measures, if any, which will be utilized at the event prior to or after receiving test results.

Huora - Appendix - 82/83 (Cassette) and real risks to the health of pigs and people from influenza infection fuels the need for the information gained from the surveillance efforts.

Testing field samples submitted under the IAV-S Surveillance Program has several immediate and long term benefits to both producers and the public. In the short-term, the information is used to make decisions addressing disease control and prevention measures, human health concerns and trade issues. In addition, researchers and the animal health industry can use the information to develop and update relevant diagnostic reagents, targeted influenza diagnostic assays, effective vaccines and response plans.

During FY October Septemberpigs were tested through diagnostic laboratory submissions from accessions. Fifty-four accessions contained mixed subtypes [ ]. An increase in swine diagnostic lab submissions through the IAV-S Surveillance Program will continue to provide valuable information to the industry, researchers and public health officials. Over the long-term, the information may be used to help understand influenza infection in pigs, to gain a better understanding of epidemiological factors affecting the mutation and spread of IAV-S in the swine population, and to provide information for broader initiatives such as Veterinary Services Project, Surveillance for Action, a stream-based comprehensive and integrated animal disease surveillance system.

Internationally from —, introductions of the H1N1pdm09 influenza virus from humans into swine were observed in 12 countries and regions. Due to the high level of surveillance and transparency, a majority of reported introductions occurred in the U. Transmission of seasonal influenza viruses from humans to swine is also being monitored in the U. From toat least 23 separate introductions were documented, with six first identified in the U.

Monitoring the transmission of influenza viruses from humans to pigs aids in understanding the contribution of human-origin influenza viruses to the genetic diversity of IAV-S. There have been several instances in the past 15 years when gene reassortment between human seasonal and swine viruses produced new IAV-S lineages that became established in the swine population [ 54 ].

When virus transmission increases between humans and pigs, measures to prevent transmission need to be followed. Increased biosecurity measures and utilization of influenza vaccination for swine workers and pigs may be necessary to lower the risk of reassortment between human and swine viruses.

A surveillance program is most useful e. The IAV-S Surveillance Program currently focuses on testing specimens submitted from swine herds affected by respiratory disease. If some regions are under-reported or over-reported it may skew the estimation of strain frequencies, which could affect the selection of widely representative vaccine strains. Complementary data could be gained through a sentinel surveillance component, which involves sampling representative herds at regular intervals, independently of disease incidence.

Sentinel surveillance could therefore help to identify a full cross-section of circulating IAV-S strains. Many different diagnostic tools are available to laboratories for the detection of influenza infection in pigs. Samples collected by producers and veterinarians are tested with pen side tests or submitted to NAHLN or private laboratories. Which test is conducted depends on the sample submitted and the tests available at that specific laboratory.

Various samples including serum, Gallardas V - Juan Cabanilles - La Bataille (Vinyl, LP, Album) tissue, nasal swabs, tissue swabs and oral fluid are being collected in the field for influenza testing. Snout wipes have recently been introduced and are still very new in the diagnostic world.

Details of each sample collection are included below. Serum collected at least one week after the start of infection may contain antibody. One week after infection, pigs may have titers of at least These titers can increase to to when sampled 14—21 days after infection [ ].

Paired samples may be especially useful in vaccinated herds. Tissue from each animal sampled should remain in an individual bag for submission. When collecting samples using nasal swabs, polyester or flocked swabs are inserted into the nasal cavity while the pig is restrained. However, if swabbed too aggressively, blood may interfere with IAV-S testing [ ] so caution should be taken in rotating too vigorously or inserting the swab too deeply.

The swab is placed in a tube containing medium or sterile saline or alternatively, the ampule at the end of the sheath is squeezed and medium is released onto the swab if applicable. Polyester or flocked swabs are inserted into small airways in lung tissue taken from post-mortem necropsy [ ]. The swab is rotated to collect surface epithelium.

The swab is placed in the tube with medium or sterile saline or alternatively, the ampule at the end of the sheath is squeezed and medium is released onto the swab if applicable. Oral fluid samples can be collected on an individual animal basis, or alternatively on a group basis by hanging ropes in pens [ ]. Cotton ropes are suspended over the pen, at shoulder height for the pig and away from feed and water. After 20—30 min, the oral fluid is extracted from the rope either by placing a plastic bag over the hanging rope and stripping the fluid from the rope into the bag or by cutting off the rope, placing it into the bag and squeezing out the fluid.

A corner of the plastic bag can be cut to allow the fluid to be collected into a plastic tube. One case study compared diagnostic results from testing nasal swabs versus snout wiping [ ]. Snout wiping is performed by using a disposable household cleaning pad soaked in saline. A corner of the bag is cut and the pad is squeezed so the liquid runs into a plastic snap tube for submission to the laboratory.

In this case study, virus isolation and sequencing were successful, and the sequencing information was utilized to help select a vaccine for breeding animals. Although this sample collection technique shows great promise, validation studies still need to be performed before snout wipes become a widely recommended sampling technique. Accurate, cost effective IAV-S diagnostic testing with a rapid turnaround time is desired by veterinarians in the field who are making recommendations for IAV-S control or prevention in swine herds.

Reliable diagnostics provide critical information to assist veterinarians in the decision making process. Several diagnostic tests are available, but laboratories vary in the tests they offer to clients. Serum HI antibodies are also considered the gold-standard correlate of protection from inactivated IAV vaccines.

This test is conducted by adding serial dilutions of the submitted serum samples to a known concentration of virus. A titer is determined by the degree to which antibodies in the serum samples bind the virus in the test plates, thus preventing agglutination of the indicator erythrocytes. Paired serum samples collected 10—21 days apart are ideal.

A titer increase of four-fold or greater between the two samples suggests a IAV-S infection [ ]. The HI test is easy and quick to perform [ ]. However, the success of this test depends on whether the virus strain used in the test and the field strain are antigenically similar, so laboratories may need to test samples against a panel of IAV-S strains [ ]. Lee et al. This indirect ELISA assay against the NP protein has gained in use in recent years due to the complexity of antigens needed for HI assays and its flexibility to test sera from multiple species.

Other serological tests developed but not commonly used include virus neutralization, agar gel immunodiffusion, and indirect fluorescent antibody assays [ ]. Influenza virus can be isolated through cell culture from lung tissue and nasal swabs [ ].

MDCK cells or primary porcine kidney cells can be utilized. This test may take 2—3 days to perform, which is longer than many virus detection methods [ ]. It is more commonly used to characterize the virus and to isolate the virus when producing autogenous vaccine rather than for routine diagnosis []. There is a short window of opportunity for IAV-S isolation from infected pigs, so isolation attempts often fail. Therefore it is important to select specific animals that are most likely to be shedding virus.

It is best to identify pigs with fever and other clinical signs [ ], but some strains of IAV-S may not cause acute disease. Selecting pigs based on a qualitative rapid detection kit e.

Egg inoculation can be performed on lung tissue and nasal swabs and has been considered one of the better methods for influenza testing due to its sensitivity [ ]. However, Swenson et al. Not all laboratories offer this test as it can be expensive Huora - Appendix - 82/83 (Cassette) maintain the supply of embryonated eggs. Another drawback is that it takes multiple days to perform as with cell culture [ ]. This test is utilized to isolate the virus when producing autogenous vaccine [ ].

The hemagglutination assay is a relatively quick assay which determines if influenza virus is present. As a stand-alone test it is not highly sensitive. However, after specimen is passaged in eggs or cell culture, hemagglutination is a rapid method to detect amplified virus. PCR can be performed on oral fluid samples for virus detection, although several substances can interfere with virus isolation [ ]. Assay development continues on oral fluid samples as they are an efficient approach to testing a large number of animals.

Overall, RT-PCR tests can be performed more quickly than cell culture or egg culture isolation of the virus, but can be more expensive. Fluorescent antibody FA testing, which detects IAV-S antigens and is performed on frozen sections of lung tissue, can be completed in hours.

However, the FA test does have its limitations. IAV-S antigens are only present in lung tissue for a short time following infection. In addition, autolytic changes in lung tissue will affect the test, so fresh lung tissue needs to be submitted [ ].

Immunohistochemistry IHC is an inexpensive, rapid and easy to perform test utilized to detect H1N1 and H3N2 influenza virus antigens on slides from formalin fixed tissue or nasal swabs [ ].

IHC testing has been shown to have sensitivity equivalent to virus isolation and greater than FA [ ]. Antigen-capture enzyme-linked immunosorbent assays ELISAs are commercially available to detect influenza in nasal swabs and lung tissue [ ].

However, excess blood and mucus on nasal swabs or freezing lung tissue may reduce the sensitivity of the test [].

Tissue swabs of airways have also been tested successfully []. These tests require a panel of reference antisera specific to each HA or NA 第一次見到你 - 太陽神樂隊* - 又是一個下雨天 (Vinyl, LP, Album) of interest.

The neuraminidase inhibition test is more cumbersome and likely to be performed mainly by reference laboratories [ ]. Complete or partial gene sequencing is often utilized to determine the subtype and genetic similarity to reference strains from the herd or to vaccine strains.

Phylogenetic relationships of IAV genes may also be determined with these sequences and used to monitor virus evolution. Samples collected from pigs under the case-compatible swine accessions or through targeted surveillance of sick pigs at first points of concentration or commingling events are tested at NAHLN laboratories while all samples associated with a human case are tested at the National Veterinary Services Laboratories NVSL in Ames, Iowa [ ].

NVSL is the confirmatory laboratory. Matrix PCR is performed on submitted samples as a screening test. A positive matrix PCR indicates influenza nucleic acid is present. If the matrix PCR is positive, diagnosticians perform subtyping PCR and virus isolation to determine which influenza virus is present.

If the subtype is undetermined for example as when a H5 isolate is being analyzedadditional testing will be utilized to subtype the virus. Virus isolation may be followed by gene sequencing. When sequencing is performed, hemagglutinin, neuraminidase and matrix genes are sequenced. Each strain of virus is cultivated in eggs or cell culture and inactivated with chemical agents, such as formaldehyde or binary ethylenimine [ ].

Inactivated viruses of multiple strains are blended and formulated with an adjuvant. Regulatory approval of an inactivated virus vaccine requires successful demonstration of safety and efficacy [ ]. Efficacy is determined by experimental challenge of seronegative animals with the strain of virus identical to each vaccine seed virus, and sometimes with a heterologous strain.

Since IAV-S strains are antigenically diverse and evolving, and many young pigs have maternal antibodies that can interfere with vaccines, the field efficacy of an approved product cannot be taken for granted. There are commercial vaccines that combine IAV-S antigens with antigens for other agents, such as Erysipelothrix rhusiopathiaeMycoplasma hyopneumoniaeLeptospira species, or porcine parvovirus. Manufacturers must demonstrate that antigens in a combination product do not interfere with each other in terms of efficacy [ ].

Conventional inactivated vaccines are effective in inducing protective immunity against antigenically identical or very similar strains [ 82]. In this ideal situation, the vaccine elicits systemic antibodies that can neutralize the virus very early without triggering extensive inflammation.

The annual strain selection process for human seasonal influenza vaccines aims for this ideal. The human seasonal vaccines are reformulated most years, based on the results of global surveillance and identification of new strains that emerged through antigenic drift or shift [].

For IAV-S, maintaining close antigenic matches in the commercial inactivated virus vaccines is more difficult. First, the evolution of swine H1 and H3 viruses in North America has resulted in co-circulating strains that belong to about seven antigenically distinct clusters within the two subtypes see Section 2. Second, IAV-S surveillance to monitor the evolution of strains within the United States is still a young program, and the geographical distribution of IAV-S genotypes across North America is far from homogenous [ ].

Third, manufacturers of IAV-S vaccines make independent decisions about the strains contained in their products, and typically do not share those strains or publish their HA gene sequences. Untilupdating strains in an IAV-S vaccine required a new licensure process for the product, including efficacy and field safety testing, which was recognized as a barrier to manufacturers making timely strain changes.

InUSDA-CVB introduced a new policy to allow manufacturers flexibility to change strains under an existing license, by either adding or replacing viruses, and demonstrating immunogenicity equivalent to that of the prior strains [ ]. Despite this move to foster better matching between vaccines and the evolving IAV-S subtypes, strain updates over the following years have not been common.

Reasons for this might include lack of confidence by firms that existing IAV-S surveillance data can identify better strains, and the time and expense required for regulatory approval, even under the revised policy.

Recent serological data strongly suggest that antigenic drift among the Cluster IV H3N2 viruses has been substantial enough to reduce efficacy of the commercial vaccines [ ]. With the strengthening of North American IAV-S surveillance in recent years [ 5157 ], data are available to support more frequent and collaborative vaccine strain decisions.

The greater valency of the newer products was a response to the emergence of antigenically distinct clusters within the H1 and H3 subtypes. This was an important development. Three of the earlier commercial vaccines that contained only a cluster I H3N2 strain were insufficient to reduce shedding of a cluster III H3N2 virus after challenge infection, whereas an experimental vaccine containing a cluster Love Me Or Leave Me - Ruth Etting - Centenary Album (CD, Album) virus conferred full protection [ ].

A more recent experimental challenge study gave similar evidence that polyvalent commercial vaccines containing cluster IV H3N2 can protect against a drifted contemporary cluster IV strain better than a commercial vaccine containing only cluster I H3N2 [ ]. Although antigenic drift is likely diminishing the quality of protection from the newer polyvalent vaccines [, ], it is reasonable to assume these will protect herds more reliably than bivalent vaccines that contain even older IAV-S strains.

It would be beneficial if practitioners had more tools at their disposal to support a best-possible match between endemic IAV-S strains and the existing commercial vaccines. When field isolates are characterized, such as by serology or HA gene sequence, it would be valuable to relate their properties directly with the strains contained in available vaccines Figure 4. If full-length HA sequences of all vaccine strains were available, one could identify which of those vaccines offers the nearest sequence homology to the field isolate of concern.

Presently, such a service is available through the University of Minnesota Veterinary Diagnostic Laboratory. Major manufacturers of IAV-S vaccines privately share the HA sequences of their proprietary seed viruses with the laboratory. Decision tree for selection of IAV-S vaccine strategy to control a specific herd isolate. Due to the diversity and rapid evolution of IAV-S, there are currently no one-size-fits-all vaccine options.

In some cases, data may indicate that commercial polyvalent vaccines offer no close matches to the field strain, suggesting a greater advantage for custom vaccines. A similar approach was reported in a case study by Corzo et al. This provided reasonable assurance that Flu-Sure XP contained HA antigen well-matched to the local circulating virus, and after mass vaccination of all breeding females the outbreak came to an end.

However, sequence homology will not necessarily predict cross-protection because some sites in HA influence antigenic properties more than others. In a recent study, six critical amino acid locations were identified in H3; substitutions at one or two of those positions were sometimes enough to markedly change cross reactivity in the HI assay [ ]. This suggests that HI or neutralization assays should be conducted in addition to sequence analysis.

One relevant way to evaluate the match between field strains and vaccine viruses is to test vaccine-induced antisera for reactivity against field isolates, using HI or neutralization assays. This enables the diagnostic laboratories to compare the serum antibodies induced by available vaccines in terms of activity against IAV-S field isolates. It is roughly parallel to the idea of antibiotic sensitivity testing, where a laboratory analyzes bacterial field isolates for inhibition by the available antibiotics, reporting the most favorable options back to the practitioner.

After conversations with diagnostic laboratories and Diversify - Ruined Conflict - A Voice For The Voiceless (CD, Album), we suggest that this approach could be adapted further by using swine antisera induced by the licensed polyvalent vaccines instead of monovalent components of the vaccineadministered in accordance with the approved product labels.

First, this would be more efficient because it only requires one test for each of the available vaccines, instead of several tests to look at monovalent components one-by-one. Second, the results might be more realistic because any interactions between the multiple strains in the vaccine positive or negative would be accounted for. Similar strategies were reported in published studies by Lee et al.

Representatives of the major IAV-S vaccine manufacturers have expressed willingness to supply interested diagnostic laboratories Élisa - Gainsbourg* - Je TAime. Moi Non Plus - 1966 À 1968 (Cassette) monovalent or polyvalent antisera induced by their vaccines.

The serological method requires isolation and propagation of virus from the herd, and therefore is not possible if diagnosis is by PCR only, or if the strain in question does not grow well in the laboratory.

Significant improvement in IAV-S vaccines in the longer term will require coordinated efforts by the various parties participating in field surveillance, strain selection, manufacturing, and product licensure. If IAV-S strains in the conventional inactivated vaccines could be updated more rapidly, in response to new trends in the surveillance data, the vaccines would have more consistent efficacy in the field. In Section 7. However, veterinary vaccine experts have outlined long-range visions of a more flexible, coordinated, and data-driven program to select IAV-S strains [].

Cooperation could be focused on several aims:. Continuous evaluation of circulating strains and their antigenic similarity to current vaccines. Representative viruses from prevalent subtypes or genotypes should be evaluated at an antigenic level by serologic cross-reactivity with vaccine anti-sera. Challenge experiments in pigs could be conducted to test for loss of vaccine efficacy when antigenic changes are identified. Strain update working group.

Manufacturers currently perform independent serology and in vivo challenge experiments, at significant cost, to assess if their polyvalent inactivated vaccines provide enough protection against circulating IAV-S strains.

If the serology, bioinformatics analysis, and challenge experiments were performed under USDA leadership, it should be a more efficient use of resources. Some IAV-S strains with desired antigenic properties are limited by poor growth properties, making them difficult to manufacture. As discussed elsewhere in the paper, antibody targets are mainly in HA and NA genes while efficient replication and protein expression in culture tend to be controlled by the internal proteins.

Traditional gene reassortment or modern reverse genetics techniques can be used to combine HA and NA genes of a new strain of interest with internal genes of a high-growth strain, making an optimal seed virus for manufacturing.

If a donor strain could be qualified in advance, receive regulatory approval, and be made available to all manufacturers, it could speed the process of making strain updates. Revise regulatory policies to accommodate new vaccine platforms, such as LAIV and recombinant viral vectored products.

Autogenous vaccines are intended for use in situations where commercial vaccines are ineffective or unavailable [ ]. Before using an autogenous vaccine, two questions to consider are whether commercial vaccines have been employed and found ineffective, and whether other barriers to vaccine efficacy, such as management factors, exist in the herd and could be contributing to the apparent lack of efficacy [ ].

A significant number of U. The primary reason for their use is thought to be the diversity of IAV-S variants circulating among pigs in North America, combined with the limited number of IAV-S strains available in commercial vaccines [ 39 ]. In the U. Ordinarily, the vaccine organism s must come from the herd in which the vaccine is to be used [ ]. Multiple isolates from the herd are commonly used in an autogenous vaccine. In addition to vaccine components from other pathogens, autogenous IAV-S vaccines may contain various combinations of H1 and H3 viruses [ ].

An autogenous vaccine is only permitted for use in the herd of origin, unless there is epidemiological evidence that adjacent or nonadjacent herds are at risk [ ]. The State Veterinarian, or equivalent state official, must be informed when an authorized vaccine is used in such herds. Autogenous vaccines are tested for safety in laboratory animals mice or guinea pigs and for purity [ ]. Purity testing includes testing for the absence of viable bacteria and fungi. Autogenous influenza vaccines must also meet the general requirements for the production of viral vaccines [].

These requirements [ ] stipulate that tests must be incorporated into the manufacturing process to ensure complete viral inactivation. However, testing is overall less rigorous than required of commercial IAV-S vaccines [ ]. In particular, manufacturers of autogenous vaccines do not need to conduct potency and efficacy testing. As a result, some vaccines might contain antigen doses that are suboptimal for that particular viral strain.

The expiration date for formulated autogenous vaccines is a maximum of 18 months after harvest [ ]. A microorganism can be used for autogenous vaccine manufacturing until 15 months after it was first isolated, or for 12 months after the date of harvest for the first serial [ ]. Extensions to 24 months are now permitted without CVB review, provided the firm maintains records documenting, among other things, that the vaccine was beneficial and that the microorganism remains associated with disease in the herd [].

With additional tests and CVB authorization, additional serials may be produced after 24 months has passed since virus isolation [ ]. Advantages of autogenous vaccines include the ability to customize the vaccine to the specific virus es in the herd, to include multiple agents, and to customize the adjuvant [ ]. When selecting a multi-agent autogenous vaccine, it should be noted that there is no requirement to test for potential interference between vaccine antigens or adjuvant components [ ].

Given the less rigorous testing requirements, an autogenous vaccine for a new viral strain can be produced and delivered much more rapidly than an updated commercial vaccine. There is nevertheless a significant lag period to isolate and characterize the agent and manufacture the vaccine, compared to ordering a commercial vaccine that is already available.

While the absence of extensive testing may also lower the price of autogenous vaccines, this comes at the cost of potential uncertainties in potency and efficacy. In addition, there is an increased risk that adventitious agents might be present in a Heaven Help The New Girl - The Long Blondes - Someone To Drive You Home (CD, Album) prepared from field viruses and not tested extensively [ ].

In addition, not all IAV-S isolates adapt well to cell culture, or grow to high titers for vaccine production. When selecting an autogenous vaccine, consideration should be given to the choice of manufacturer, as the products produced by different companies may vary.

A complete economic evaluation, including performance, morbidity and mortality, can help determine the cost savings or loss from vaccine use; the selection of a vaccine should not be based solely on price [ ]. A vaccine trial can help evaluate whether the commercial or autogenous vaccine is more effective in the herd [ ]. It is highly recommended that post-vaccination sera be collected to test against the herd IAV-S strains contained in the autogenous vaccine for serologic evidence to support vaccine efficacy.

The efficacy of autogenous vaccines against IAV-S has not been evaluated and reported to a significant extent in the literature. All three vaccines provided partial protection against this virus, although all were less effective than an experimental vaccine containing a virus identical to the challenge strain.

It is likely that autogenous and commercial vaccine efficacy will differ between herds, depending on the specific viruses that affect those herds. Certain vaccines for other mammalian viruses have been shown to induce immune responses that later exacerbate the severity of infection [ ]. With influenza viruses, vaccine failure has usually been equated with little or no protective immunity and lack of prevention of virus transmission in the herd rather than disease exacerbation.

However, in vivo experiments in recent years have revealed a potentially important phenomenon of vaccine associated enhanced respiratory disease VAERD in IAV-S infected pigs. VAERD has been observed in pigs immunized with an adjuvanted, whole inactivated, monovalent IAV-S vaccine and later challenged with an antigenically divergent strain still of the same subtype [ 3883]. Serum IgG antibodies induced by the vaccine bind to the heterologous challenge virus strain, but provide no significant cross-neutralization.

Histological examination of VAERD-affected lung reveals more prominent bronchiolitis, peribronchiolar lymphocytic cuffing, and interstitial pneumonia [ 38].

VAERD may be the result of multifactorial mechanisms, including dysregulation of proinflammatory cytokines and immune cell types. However, one consistent component seems to be vaccine-induced cross-reactive IgG antibodies in the absence of HI or neutralizing antibodies [ 3883]. Such cross-reactive IgG antibodies might activate inflammatory immune mechanisms that damage tissues without efficient control of virus replication. In vitro assays with serum from VAERD-affected pigs showed evidence that these IgG antibodies bind to the heterologous strain but fail to neutralize it and instead promote virus infectivity and fusion, thus leading to elevated replication [ ].

In one study, pigs that were inoculated with live, wild-type virus were partially protected from heterologous challenge infection, whereas the group that received a whole inactivated virus vaccine of the same strain went on to develop VAERD after challenge [ 83 ]. A different study tested whether a live attenuated influenza virus LAIV vaccine presenting the same H1N2 surface antigens as the whole inactivated virus vaccine would also potentiate VAERD after heterologous pandemic H1N1 challenge [ ].

In contrast, the LAIV vaccine conferred significant cross-protection against viral replication and disease. The pronounced difference between inactivated and live vaccines likely results from superior induction of cell-mediated and mucosal immunity with the LAIV vaccine. An additional recent study tested whether VAERD would occur in piglets that received maternal antibodies from whole inactivated virus WIV -vaccinated sows, prior to challenge with the heterologous virus [ ].

This result points to IgG antibodies as the immune mediator mainly responsible for triggering VAERD as opposed to T lymphocytesand also raises a note of caution about immunizing breeding sows with WIV vaccines if antigenic relevance of vaccine strains is in doubt.

These vaccines encoded M2e the highly conserved, extracellular domain of the M2 protein and induced non-neutralizing antibodies against it [ 32 ].

The relevance of this experiment to VAERD induced by inactivated virus vaccines is uncertain, although it is possible that the underlying mechanisms causing lung lesions are similar. To our knowledge, VAERD has not yet been definitively demonstrated in IAV-S-infected swine herds, although it is inherently difficult to make such a determination under field conditions.

Conventionally licensed and autogenous vaccines used in the field contain inactivated viruses with adjuvant, and many circulating IAV-S strains are antigenically distinct from the vaccines, so it is a realistic possibility. On the other hand, vaccines in the VAERD experiments were monovalent, whereas polyvalent commercial vaccines contain antigens from multiple H1 and H3 clusters.

Since VAERD pathogenesis requires a major antigenic difference between vaccine and challenge virus i. Data from two studies where pigs were vaccinated with multivalent commercial vaccines before challenge with pandemic H1N1 virus, with no report of VAERD, support this idea []. Natural infection also differs from the experimental setting in the route of exposure: droplet transmission from animal to animal, versus intratracheal or intranasal inoculation.

Thus the VAERD studies, like most animal experiments, simplify some of the complex conditions found in the field to make the outcomes more reproducible. It is nevertheless prudent to take vaccine-enhanced disease into account as a possible hazard to herd health, and consider ways to lower that risk.

The preference for a vaccine with the best-possible antigenic match, even if it is not a full match, holds true with respect to avoiding VAERD. Ideas mentioned above for optimal protection included comparing gene sequence of field isolates and vaccine seed viruses, or developing antisera to commercial vaccines that would enable serological tests against field strains Section 7.

Both of these would be useful ways to identify the most relevant vaccine option and reduce the risk of VAERD. Also, a polyvalent vaccine that contains representatives of multiple H1 and H3 clusters would be less likely to potentiate VAERD than a bivalent vaccine with only one older, antigenically distant strain of each subtype. Autogenous vaccines provide assurance that the currently circulating strain will be well matched to the vaccine and unlikely to cause VAERD.

The drawback is that a new strain belonging to an antigenically divergent cluster could emerge or co-circulate, in which case antibodies already induced by the autogenous vaccine might predispose pigs to VAERD. Perhaps the most stringent way to supply protection and prevent VAERD is to immunize with an autogenous vaccine to control the locally predominant virus plus multivalent commercial vaccine to control other strains that may enter the herd.

The vector is a modified form of Huora - Appendix - 82/83 (Cassette) attenuated Venezuelan equine encephalitis virus, from which structural genes have been deleted, thus preventing multi-cycle replication of the virus reviewed by Vander Veen et al.

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