Human infection with highly pathogenic A(H7N7) avian influenza virus, Italy, 2013.
Ontology highlight
ABSTRACT:
SUBMITTER: Puzelli S
PROVIDER: S-EPMC4193179 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:H7 avian influenza viruses represent a major public health concern, and worldwide outbreaks raise the risk of a potential pandemic. Understanding the memory B cell response to avian (H7) influenza virus infection in humans could provide insights in the potential key to human infection risks. We investigated an epizootic of the highly pathogenic A(H7N7) in the Netherlands, which in 2003 led to infection of 89 persons and one fatal case. Subtype-specificity of antibodies were determined for confirmed H7N7 infected individuals (cases) (n = 19), contacts of these cases (n = 21) and a comparison group controls (n = 16), by microarray, using recombinant hemagglutinin (HA)1 proteins. The frequency and specificity of memory B cells was determined by detecting subtype-specific antibodies in the culture supernatants from in vitro stimulated oligoclonal B cell cultures, from peripheral blood of cases and controls. All cases (100%) had high antibody titers specific for A(H7N7)2003 (GMT > 100), whereas H7-HA1 antigen binding was detected in 29% of contacts and 31% of controls, suggesting that some of the H7 reactivity stems from cross reactive antibodies. To unravel homotypic and heterotypic responses, the frequency and specificity of memory B cells were determined in 2 cases. Ten of 123 HA1 reactive clones isolated from the cases bound to only H7- HA1, whereas 5 bound both H7 and other HA1 antigens. We recovered at least four different epitopal reactivities, though none of the H7 reactive antibodies were able to neutralize H7 infections in vitro. Our study serologically confirms the infection with H7 avian influenza viruses, and shows that H7 infection triggers a mixture of strain -specific and cross-reactive antibodies.
| S-EPMC7035254 | biostudies-literature
Project description:Although increasing data have become available that link human adaptation with specific molecular changes in nonhuman influenza viruses, the molecular changes of these viruses during a large highly pathogenic avian influenza virus (HPAI) outbreak in poultry along with avian-to-human transmission have never been documented. By comprehensive virologic analysis of combined veterinary and human samples obtained during a large HPAI A (H7N7) outbreak in the Netherlands in 2003, we mapped the acquisition of human adaptation markers to identify the public health risk associated with an HPAI outbreak in poultry. Full-length hemagglutinin (HA), neuraminidase (NA), and PB2 sequencing of A (H7N7) viruses obtained from 45 human cases showed amino acid variations at different codons in HA (n=20), NA (n=23), and PB2 (n=23). Identification of the avian sources of human virus infections based on 232 farm sequences demonstrated that for each gene about 50% of the variation was already present in poultry. Polygenic accumulation and farm-to-farm spread of known virulence and human adaptation markers in A (H7N7) virus-infected poultry occurred prior to farm-to-human transmission. These include the independent emergence of HA A143T mutants, accumulation of four NA mutations, and farm-to-farm spread of virus variants harboring mammalian host determinants D701N and S714I in PB2. This implies that HPAI viruses with pandemic potential can emerge directly from poultry. Since the public health risk of an avian influenza virus outbreak in poultry can rapidly change, we recommend virologic monitoring for human adaptation markers among poultry as well as among humans during the course of an outbreak in poultry.
| S-EPMC3187520 | biostudies-literature
Project description:The recent increase in zoonotic avian influenza A(H7N9) disease in China is a cause of public health concern. Most of the A(H7N9) viruses previously reported have been of low pathogenicity. We report the fatal case of a patient in China who was infected with an A(H7N9) virus having a polybasic amino acid sequence at its hemagglutinin cleavage site (PEVPKRKRTAR/GL), a sequence suggestive of high pathogenicity in birds. Its neuraminidase also had R292K, an amino acid change known to be associated with neuraminidase inhibitor resistance. Both of these molecular features might have contributed to the patient's adverse clinical outcome. The patient had a history of exposure to sick and dying poultry, and his close contacts had no evidence of A(H7N9) disease, suggesting human-to-human transmission did not occur. Enhanced surveillance is needed to determine whether this highly pathogenic avian influenza A(H7N9) virus will continue to spread.
| S-EPMC5547808 | biostudies-literature
Project description:Outbreaks of highly pathogenic avian influenza virus (HPAIV) often result in the infection of millions of poultry, causing up to 100% mortality. HPAIV has been shown to emerge from low pathogenicity avian influenza virus (LPAIV) in field outbreaks. Direct evidence for the emergence of H7N7 HPAIV from a LPAIV precursor with a rare di-basic cleavage site (DBCS) was identified in the UK in 2008. The DBCS contained an additional basic amino acid compared to commonly circulating LPAIVs that harbor a single-basic amino acid at the cleavage site (SBCS). Using reverse genetics, outbreak HPAIVs were rescued with a DBCS (H7N7DB), as seen in the LPAIV precursor or an SBCS representative of common H7 LPAIVs (H7N7SB). Passage of H7N7DB in chicken embryo tissues showed spontaneous evolution to a HPAIV. In contrast, deep sequencing of extracts from embryo tissues in which H7N7SB was serially passaged showed retention of the LPAIV genotype. Thus, in chicken embryos, an H7N7 virus containing a DBCS appears naturally unstable, enabling rapid evolution to HPAIV. Evaluation in embryo tissue presents a useful approach to study AIV evolution and allows a laboratory-based dissection of molecular mechanisms behind the emergence of HPAIV.
| S-EPMC7552004 | biostudies-literature
Project description:Estimates of the per-contact probability of transmission between farms of Highly Pathogenic Avian Influenza virus of H7N7 subtype during the 2003 epidemic in the Netherlands are important for the design of better control and biosecurity strategies. We used standardized data collected during the epidemic and a model to extract data for untraced contacts based on the daily number of infectious farms within a given distance of a susceptible farm. With these data, we used a maximum likelihood estimation approach to estimate the transmission probabilities by the individual contact types, both traced and untraced. The estimated conditional probabilities, conditional on the contact originating from an infectious farm, of virus transmission were: 0.000057 per infectious farm within 1 km per day, 0.000413 per infectious farm between 1 and 3 km per day, 0.0000895 per infectious farm between 3 and 10 km per day, 0.0011 per crisis organisation contact, 0.0414 per feed delivery contact, 0.308 per egg transport contact, 0.133 per other-professional contact and, 0.246 per rendering contact. We validate these outcomes against literature data on virus genetic sequences for outbreak farms. These estimates can be used to inform further studies on the role that improved biosecurity between contacts and/or contact frequency reduction can play in eliminating between-farm spread of the virus during future epidemics. The findings also highlight the need to; 1) understand the routes underlying the infections without traced contacts and, 2) to review whether the contact-tracing protocol is exhaustive in relation to all the farm's day-to-day activities and practices.
| S-EPMC3396644 | biostudies-literature
Project description:H7N7 avian influenza virus (AIV) can divided into low-pathogenic AIV and high-pathogenic AIV groups. It has been shown to infect humans and animals. Its prevalence state in wild birds in China remains largely unclear. In this study, a new strain of H7N7 AIV, designated CM1216, isolated from wild birds in Shanghai, China, was characterized. Phylogenetic and nucleotide sequence analyses of CM1216 revealed that HA, NA, PB1, NP, and M genes shared the highest nucleotide identity with the Japan H7 subtype AIV circulated in 2019; the PB2 and PA genes shared the highest nucleotide identity with the Korea H7 subtype AIV circulated in wild birds in 2018, while NS gene of CM1216 was 98.93% identical to that of the duck AIV circulating in Bangladesh, and they all belong to the Eurasian lineage. A Bayesian phylogenetic reconstruction of the 2 surface genes of CM1216 showed that multiple reassortments might have occurred in 2015. Mutations were found in HA (A135 T, T136S, and T160 A [H3 numbering]), M1 (N30D and T215 A), NS1 (P42S and D97 E), PB2 (R389 K), and PA (N383D) proteins; these mutations have been shown to be related to mammalian adaptation and changes in virulence of AIVs. Infection studies demonstrated that CM1216 could infect mice and cause symptoms characteristic of influenza virus infection and proliferate in the lungs without prior adaption. This study demonstrates the need for routine surveillance of AIVs in wild birds and detection of their evolution to become a virus with high pathogenicity and ability to infect humans.
| S-EPMC7858150 | biostudies-literature
Project description:Subclinical infection of vaccinated chickens with a highly pathogenic avian influenza A(H5N2) virus was identified through routine surveillance in China. Investigation suggested that the virus has evolved into multiple genotypes. To better control transmission of the virus, we recommend a strengthened program of education, biosecurity, rapid diagnostics, surveillance, and elimination of infected poultry.
| S-EPMC4257838 | biostudies-literature
Project description:During the highly pathogenic avian influenza (HPAI) H5N8 virus outbreak in Korea, a dog in layer farm contaminated by H5N8 was reported seropositive for HPAI H5N8. To investigate the possibility of adaptation and transmission of HPAI H5N8 to dogs, we experimentally inoculated dogs with H5N8. Viral genes were weakly detected in nasal swabs and seroconversions in inoculated and contact dogs. Although the H5N8 virus did not induced severe clinical signs to dogs, the results suggest that surveillance of farm dogs should continue as a species in which the avian influenza virus may acquire infectivity to mammals through frequent contact with the virus.
| S-EPMC5583426 | biostudies-literature
Project description:Two viruses isolated during the highly pathogenic avian influenza (HPAI) H7N7 virus outbreak in The Netherlands in 2003, one isolated from a person with conjunctivitis and one from a person who died as the result of infection, were used for an in vitro study of influenza A virus pathogenicity factors. The two HPAI H7N7 viruses differed in 15 amino acid positions in five gene segments. Assays were designed to investigate the role of each of these substitutions in attachment and entry, transcription and genome replication, and virus production and release as determined by hemagglutinin (HA), polymerase proteins, nonstructural protein 1 (NS1), and neuraminidase (NA). These in vitro studies confirmed the roles of the E627K substitution in basic polymerase 2 (PB2) and the A143T substitution in HA in pathogenicity observed in a mouse model previously. However, the in vitro studies identified a contribution of acidic polymerase (PA) and NA to the efficient replication in human cells of the fatal case virus, despite the fact that these are rarely marked as determinants of pathogenicity in in vivo studies. With the exception of PB2 E627K, all substitutions contributing to enhanced replication of the fatal case virus in vitro were present in poultry viruses prior to transmission to the human fatal case, indicating that viruses with enhanced replication efficiency in the mammalian host can be generated in poultry. Thus, detailed in vitro analyses of mutations facilitating replication of avian influenza viruses in mammalian cells are important to assess the zoonotic risk posed by these viruses and, in addition, highlight the value of in vitro studies to complement animal models.
| S-EPMC2812334 | biostudies-literature
Project description:Over the last decade, more than half of humans infected with highly pathogenic avian influenza (HPAI) H5N1 viruses have died, and yet virus-induced host signaling has yet to be clearly elucidated. Airway epithelia are known to produce inflammatory mediators that contribute to HPAI H5N1-mediated pathogenicity, but a comprehensive analysis of the host response in this cell type is lacking. Here, we leveraged a systems biology method called weighted gene correlation network analysis (WGCNA) to identify and statistically validate signaling sub-networks that define the dynamic transcriptional response of human bronchial epithelial cells after infection with influenza A/Vietnam/1203/2004 (H5N1, VN1203). A detailed examination of two sub-networks involved in the immune response and keratin filament formation revealed potential novel mediators of HPAI H5N1 pathogenesis, and additional experiments validated upregulation of these transcripts in response to VN1203 infection in C57BL/6 mice. Using emergent network properties, we provide fresh insight into the host response to HPAI H5N1 virus infection, and identify novel avenues for perturbation studies and potential therapeutic intervention of fatal HPAI H5N1 disease.
2011-09-02 | GSE28166 | GEO