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Related Experiment Video

Updated: Dec 15, 2025

Using Zebrafish Models of Human Influenza A Virus Infections to Screen Antiviral Drugs and Characterize Host Immune Cell Responses

Using Zebrafish Models of Human Influenza A Virus Infections to Screen Antiviral Drugs and Characterize Host Immune Cell Responses

Published on: January 20, 2017

Collective interactions augment influenza A virus replication in a host-dependent manner.

Kara L Phipps¹, Ketaki Ganti¹, Nathan T Jacobs¹

¹Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, USA.

Nature Microbiology

|July 8, 2020

Summary

Influenza A virus (IAV) requires multiple viral genomes for infection, forming a species barrier. Avian H9N2 IAV shows high dependence on this in mammals, driven by the PA gene segment.

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Last Updated: Dec 15, 2025

Using Zebrafish Models of Human Influenza A Virus Infections to Screen Antiviral Drugs and Characterize Host Immune Cell Responses

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Published on: January 20, 2017

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Affinity Purification of Influenza Virus Ribonucleoprotein Complexes from the Chromatin of Infected Cells

Affinity Purification of Influenza Virus Ribonucleoprotein Complexes from the Chromatin of Infected Cells

Published on: June 3, 2012

Area of Science:

Virology
Molecular Biology
Evolutionary Biology

Background:

Productive infection by influenza A virus (IAV) often necessitates multiple viral genomes within a single cell, rather than a single virion.
This reliance on multiple infection is a critical factor in understanding viral transmission and host adaptation.

Purpose of the Study:

To investigate the role of multiple IAV infection in forming species barriers, particularly for avian H9N2 viruses at the poultry-human interface.
To elucidate the mechanisms underlying the increased dependence on multiple infection in mammalian systems compared to avian hosts.

Main Methods:

Quantification of incomplete viral genomes in avian and mammalian cells infected with avian H9N2 IAV.
Analysis of viral replication and transcription, focusing on the impact of the PA gene segment.
Comparative assessment of multiple infection reliance in natural (avian) versus non-natural (mammalian) hosts.

Main Results:

Avian H9N2 IAV exhibits a significant dependence on multiple infection in mammalian cells, a reliance less pronounced in avian cells.
Complementation of incomplete viral genomes explains moderate multiple infection reliance in avian cells but not the heightened need in mammalian cells.
The PA gene segment was identified as a key driver of this increased reliance on multiple infection in mammals, affecting both viral replication and transcription.

Conclusions:

The reliance of IAV on multiple infection acts as a significant species barrier, particularly for avian strains attempting to adapt to mammalian hosts.
Distinct mechanisms, including virus-virus interactions mediated by the PA gene segment, contribute to the heightened need for multiple infection in mammalian systems.
Understanding these virus-virus interactions is crucial for predicting IAV evolution, emergence, and potential pandemic threats.