Migratory Status Is Not Related to the Susceptibility to HPAIV H5N1 in an Insectivorous Passerine Species

Kalthoff, Donata; Breithaupt, Angele; Helm, Barbara; Teifke, Jens Peter; Beer, Martin

doi:10.1371/journal.pone.0006170

Cited by 7 publications

(12 citation statements)

References 39 publications

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“…Immunohistochemical detection of influenza A virus nucleoprotein (NP) and hematoxylin eosin staining was performed as described [58].…”

Section: Methodsmentioning

confidence: 99%

“…Samples from cerebellum, cerebrum, lung, nose, trachea, caecum, duodenum, kidney, and pancreas of additionally infected chicken were taken on day 4 and 10 post infection, formalin-fixed and processed for paraffin-wax-embedding according to standardized procedures. Immunohistochemical detection of influenza A virus nucleoprotein (NP) and hematoxylin eosin staining was performed as described [58] .…”

Section: Methodsmentioning

confidence: 99%

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Highly Pathogenic H5N1 Influenza Viruses Carry Virulence Determinants beyond the Polybasic Hemagglutinin Cleavage Site

et al. 2010

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Highly pathogenic avian influenza viruses (HPAIV) originate from avirulent precursors but differ from all other influenza viruses by the presence of a polybasic cleavage site in their hemagglutinins (HA) of subtype H5 or H7. In this study, we investigated the ability of a low-pathogenic avian H5N1 strain to transform into an HPAIV. Using reverse genetics, we replaced the monobasic HA cleavage site of the low-pathogenic strain A/Teal/Germany/Wv632/2005 (H5N1) (TG05) by a polybasic motif from an HPAIV (TG05poly). To elucidate the virulence potential of all viral genes of HPAIV, we generated two reassortants carrying the HA from the HPAIV A/Swan/Germany/R65/06 (H5N1) (R65) plus the remaining genes from TG05 (TG05-HAR65) or in reversed composition the mutated TG05 HA plus the R65 genes (R65-HATG05poly). In vitro, TG05poly and both reassortants were able to replicate without the addition of trypsin, which is characteristic for HPAIV. Moreover, in contrast to avirulent TG05, the variants TG05poly, TG05-HAR65, and R65-HATG05poly are pathogenic in chicken to an increasing degree. Whereas the HA cleavage site mutant TG05poly led to temporary non-lethal disease in all animals, the reassortant TG05-HAR65 caused death in 3 of 10 animals. Furthermore, the reassortant R65-HATG05poly displayed the highest lethality as 8 of 10 chickens died, resembling “natural” HPAIV strains. Taken together, acquisition of a polybasic HA cleavage site is only one necessary step for evolution of low-pathogenic H5N1 strains into HPAIV. However, these low-pathogenic strains may already have cryptic virulence potential. Moreover, besides the polybasic cleavage site, the additional virulence determinants of H5N1 HPAIV are located within the HA itself and in other viral proteins.

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“…Immunohistochemical detection of influenza A virus nucleoprotein (NP) and hematoxylin eosin staining was performed as described [58].…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Highly Pathogenic H5N1 Influenza Viruses Carry Virulence Determinants beyond the Polybasic Hemagglutinin Cleavage Site

et al. 2010

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“…Since the Ct values were fairly high, we estimate that our copy number is uniformly low across the passerine samples. (Ct values >35 are typically interpreted as indicating the absence of influenza in passerines [ 52 ].)…”

Section: Methodsmentioning

confidence: 99%

Mapping the risk of avian influenza in wild birds in the US

et al. 2010

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BackgroundAvian influenza virus (AIV) is an important public health issue because pandemic influenza viruses in people have contained genes from viruses that infect birds. The H5 and H7 AIV subtypes have periodically mutated from low pathogenicity to high pathogenicity form. Analysis of the geographic distribution of AIV can identify areas where reassortment events might occur and how high pathogenicity influenza might travel if it enters wild bird populations in the US. Modelling the number of AIV cases is important because the rate of co-infection with multiple AIV subtypes increases with the number of cases and co-infection is the source of reassortment events that give rise to new strains of influenza, which occurred before the 1968 pandemic. Aquatic birds in the orders Anseriformes and Charadriiformes have been recognized as reservoirs of AIV since the 1970s. However, little is known about influenza prevalence in terrestrial birds in the order Passeriformes. Since passerines share the same habitat as poultry, they may be more effective transmitters of the disease to humans than aquatic birds. We analyze 152 passerine species including the American Robin (Turdus migratorius) and Swainson's Thrush (Catharus ustulatus).MethodsWe formulate a regression model to predict AIV cases throughout the US at the county scale as a function of 12 environmental variables, sampling effort, and proximity to other counties with influenza outbreaks. Our analysis did not distinguish between types of influenza, including low or highly pathogenic forms.ResultsAnalysis of 13,046 cloacal samples collected from 225 bird species in 41 US states between 2005 and 2008 indicates that the average prevalence of influenza in passerines is greater than the prevalence in eight other avian orders. Our regression model identifies the Great Plains and the Pacific Northwest as high-risk areas for AIV. Highly significant predictors of AIV include the amount of harvested cropland and the first day of the year when a county is snow free.ConclusionsAlthough the prevalence of influenza in waterfowl has long been appreciated, we show that 22 species of song birds and perching birds (order Passeriformes) are influenza reservoirs in the contiguous US.

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“…On the other hand, increased probability of development of clinical disease may hamper such spread, as infected birds may become unable to undertake migration, or fly long distances [11] . Although stonechats ( Saxicola torquata ) exhibiting variable migratory behavior (from highly migratory to resident) were found equally susceptible to experimental HPAIV H5N1 infection at the time of migration [26] , little is known on the impact of corticosterone on influenza virus infection in wild birds.…”

Section: Introductionmentioning

confidence: 99%

Highly Pathogenic Avian Influenza Virus H5N1 Infection in a Long-Distance Migrant Shorebird under Migratory and Non-Migratory States

et al. 2011

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Corticosterone regulates physiological changes preparing wild birds for migration. It also modulates the immune system and may lead to increased susceptibility to infection, with implications for the spread of pathogens, including highly pathogenic avian influenza virus (HPAIV) H5N1. The red knot (Calidris canutus islandica) displays migratory changes in captivity and was used as a model to assess the effect of high plasma concentration of corticosterone on HPAIV H5N1 infection. We inoculated knots during pre-migration (N = 6), fueling (N = 5), migration (N = 9) and post-migration periods (N = 6). Knots from all groups shed similar viral titers for up to 5 days post-inoculation (dpi), peaking at 1 to 3 dpi. Lesions of acute encephalitis, associated with virus replication in neurons, were seen in 1 to 2 knots per group, leading to neurological disease and death at 5 to 11 dpi. Therefore, the risk of HPAIV H5N1 infection in wild birds and of potential transmission between wild birds and poultry may be similar at different times of the year, irrespective of wild birds' migratory status. However, in knots inoculated during the migration period, viral shedding levels positively correlated with pre-inoculation plasma concentration of corticosterone. Of these, knots that did not become productively infected had lower plasma concentration of corticosterone. Conversely, elevated plasma concentration of corticosterone did not result in an increased probability to develop clinical disease. These results suggest that birds with elevated plasma concentration of corticosterone at the time of migration (ready to migrate) may be more susceptible to acquisition of infection and shed higher viral titers—before the onset of clinical disease—than birds with low concentration of corticosterone (not ready for take-off). Yet, they may not be more prone to the development of clinical disease. Therefore, assuming no effect of sub-clinical infection on the likelihood of migratory take-off, this may favor the spread of HPAIV H5N1 by migratory birds over long distances.

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Migratory Status Is Not Related to the Susceptibility to HPAIV H5N1 in an Insectivorous Passerine Species

Cited by 7 publications

References 39 publications

Highly Pathogenic H5N1 Influenza Viruses Carry Virulence Determinants beyond the Polybasic Hemagglutinin Cleavage Site

Highly Pathogenic H5N1 Influenza Viruses Carry Virulence Determinants beyond the Polybasic Hemagglutinin Cleavage Site

Mapping the risk of avian influenza in wild birds in the US

Highly Pathogenic Avian Influenza Virus H5N1 Infection in a Long-Distance Migrant Shorebird under Migratory and Non-Migratory States

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