H5N1 Influenza A Virus and Infected Human Plasma

Chutinimitkul, Salin; Bhattarakosol, Parvapan; Srisuratanon, Surangrat; Eiamudomkan, Atthapon; Kongsomboon, Kittipong; Damrongwatanapokin, Sudarat; Chaisingh, Arunee; Suwannakarn, Kamol; Chieochansin, Thaweesak; Theamboonlers, Apiradee; Poovorawan, Yong

doi:10.3201/eid1206.060227

Cited by 64 publications

(50 citation statements)

References 9 publications

(11 reference statements)

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“…A high proportion of blood mDCs were infected by H5N1 virus and this subset of blood cells could represent another site of viral production leading to increased and sustained viremia. Indeed, in blood of patients, large amounts of viable H5N1 viruses were detected (4,5). The pantropic nature of H5N1 virus would thus support a systemic disease.…”

Section: Discussionmentioning

confidence: 99%

“…Unlike most influenza infections, which are limited to respiratory system, H5N1 infection causes a systemic disease. In infected patients, viral RNA and viable viruses were detected in blood specimens (4,5), suggesting that H5N1 viruses could spread beyond the primary site of infection in the lungs and cause blood-borne systemic infection. This is in agreement with the few available histopathological reports of deceased patients, which document the presence of H5N1 virus in multiple damaged organs (6 -11).…”

mentioning

confidence: 99%

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High Susceptibility of Human Dendritic Cells to Avian Influenza H5N1 Virus Infection and Protection by IFN-α and TLR Ligands

Thitithanyanont

Engering

Ekchariyawat

et al. 2007

The Journal of Immunology

102

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There is worldwide concern that the avian influenza H5N1 virus, with a mortality rate of >50%, might cause the next influenza pandemic. Unlike most other influenza infections, H5N1 infection causes a systemic disease. The underlying mechanisms for this effect are still unclear. In this study, we investigate the interplay between avian influenza H5N1 and human dendritic cells (DC). We showed that H5N1 virus can infect and replicate in monocyte-derived and blood myeloid DC, leading to cell death. These results suggest that H5N1 escapes viral-specific immunity, and could disseminate via DC. In contrast, blood pDC were resistant to infection and produced high amounts of IFN-α. Addition of this cytokine to monocyte-derived DC or pretreatment with TLR ligands protected against infection and the cytopathic effects of H5N1 virus.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

High Susceptibility of Human Dendritic Cells to Avian Influenza H5N1 Virus Infection and Protection by IFN-α and TLR Ligands

Thitithanyanont

Engering

Ekchariyawat

et al. 2007

The Journal of Immunology

102

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“…Many studies examining H5N1 infection of ferrets (39) and humans (19,22,24,53) have attempted to delineate the association between hematogenous spread of the virus and severe disease outcomes. These studies have not measured infectious viral loads in blood but, rather, have quantified vRNA copy numbers by realtime PCR.…”

Section: Discussionmentioning

confidence: 99%

Predicting Disease Severity and Viral Spread of H5N1 Influenza Virus in Ferrets in the Context of Natural Exposure Routes

Edenborough

Lowther

Laurie

et al. 2016

J Virol

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Although avian H5N1 influenza virus has yet to develop the capacity for human-to-human spread, the severity of the rare cases of human infection has warranted intensive follow-up of potentially exposed individuals that may require antiviral prophylaxis. For countries where antiviral drugs are limited, the World Health Organization (WHO) has developed a risk categorization for different levels of exposure to environmental, poultry, or human sources of infection. While these take into account the infection source, they do not account for the likely mode of virus entry that the individual may have experienced from that source and how this could affect the disease outcome. Knowledge of the kinetics and spread of virus after natural routes of exposure may further inform the risk of infection, as well as the likely disease severity. Using the ferret model of H5N1 infection, we compared the commonly used but artificial inoculation method that saturates the total respiratory tract (TRT) with virus to upper respiratory tract (URT) and oral routes of delivery, those likely to be encountered by humans in nature. We show that there was no statistically significant difference in survival rate with the different routes of infection, but the disease characteristics were somewhat different. Following URT infection, viral spread to systemic organs was comparatively delayed and more focal than after TRT infection. By both routes, severe disease was associated with early viremia and central nervous system infection. After oral exposure to the virus, mild infections were common suggesting consumption of virus-contaminated liquids may be associated with seroconversion in the absence of severe disease. IMPORTANCERisks for human H5N1 infection include direct contact with infected birds and frequenting contaminated environments. We used H5N1 ferret infection models to show that breathing in the virus was more likely to produce clinical infection than swallowing contaminated liquid. We also showed that virus could spread from the respiratory tract to the brain, which was associated with end-stage disease, and very early viremia provided a marker for this. With upper respiratory tract exposure, infection of the brain was common but hard to detect, suggesting that human neurological infections might be typically undetected at autopsy. However, viral spread to systemic sites was slower after exposure to virus by this route than when virus was additionally delivered to the lungs, providing a better therapeutic window. In addition to exposure history, early parameters of infection, such as viremia, could help prioritize antiviral treatments for patients most at risk of succumbing to infection. Since the emergence of highly pathogenic avian influenza H5N1 in humans in 1997, outbreaks have occurred sporadically, primarily in populations associated with direct contact with sick birds (1-4). Currently, outbreaks occur in regions where H5N1 is endemic in migratory birds and where a large proportion of the population rear backyard poultry ...

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“…Recent virological and immunological investigations in H5N1 patients further support that the fatal outcome is associated with high virus replication in the respiratory tract and the resulting hypercytokinemia [11]. In several H5N1 patients, infectious virus or viral RNA have also been recovered from serum or plasma, cerebrospinal fluid or gastrointestinal samples [6,9,11,52]. Non-respiratory signs and diarrhoea in particular have also been reported in some patients.…”

Section: Human Infections With Avian Influenzamentioning

confidence: 96%

Avian and swine influenza viruses: our current understanding of the zoonotic risk

2007

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H5N1 Influenza A Virus and Infected Human Plasma

Cited by 64 publications

References 9 publications

High Susceptibility of Human Dendritic Cells to Avian Influenza H5N1 Virus Infection and Protection by IFN-α and TLR Ligands

High Susceptibility of Human Dendritic Cells to Avian Influenza H5N1 Virus Infection and Protection by IFN-α and TLR Ligands

Predicting Disease Severity and Viral Spread of H5N1 Influenza Virus in Ferrets in the Context of Natural Exposure Routes

Avian and swine influenza viruses: our current understanding of the zoonotic risk

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