Involvement of annexin V in the entry of influenza viruses and role of phospholipids in infection

Huang, Richard T. C.; Lichtenberg, Beate; Rick, Oliver

doi:10.1016/0014-5793(96)00783-1

Cited by 42 publications

(26 citation statements)

References 21 publications

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“…These results differ from a previous study, which suggested that A5 could serve as a second receptor for viral entry (48). The precise physiological role of A5 remains to be determined.…”

Section: Discussioncontrasting

confidence: 99%

Annexin V Incorporated into Influenza Virus Particles Inhibits Gamma Interferon Signaling and Promotes Viral Replication

Berri

Haffar

Lê

et al. 2014

J Virol

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During the budding process, influenza A viruses (IAVs) incorporate multiple host cell membrane proteins. However, for most of them, their significance in viral morphogenesis and infectivity remains unknown. We demonstrate here that the expression of annexin V (A5) is upregulated at the cell surface upon IAV infection and that a substantial proportion of the protein is present in lipid rafts, the site of virus budding. Western blotting and immunogold analysis of highly purified IAV particles showed the presence of A5 in the virion. Significantly, gamma interferon (IFN-␥)-induced Stat phosphorylation and IFN-␥-induced 10-kDa protein (IP-10) production in macrophage-derived THP-1 cells was inhibited by purified IAV particles. Disruption of the IFN-␥ signaling pathway was A5 dependent since downregulation of its expression or its blockage reversed the inhibition and resulted in decreased viral replication in vitro. The functional significance of these results was also observed in vivo. Thus, IAVs can subvert the IFN-␥ antiviral immune response by incorporating A5 into their envelope during the budding process. IMPORTANCEMany enveloped viruses, including influenza A viruses, bud from the plasma membrane of their host cells and incorporate cellular surface proteins into viral particles. However, for the vast majority of these proteins, only the observation of their incorporation has been reported. We demonstrate here that the host protein annexin V is specifically incorporated into influenza virus particles during the budding process. Importantly, we showed that packaged annexin V counteracted the antiviral activity of gamma interferon in vitro and in vivo. Thus, these results showed that annexin V incorporated in the viral envelope of influenza viruses allow viral escape from immune surveillance. Understanding the role of host incorporated protein into virions may reveal how enveloped RNA viruses hijack the host cell machinery for their own purposes.

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“…These results differ from a previous study, which suggested that A5 could serve as a second receptor for viral entry (48). The precise physiological role of A5 remains to be determined.…”

Section: Discussioncontrasting

confidence: 99%

Annexin V Incorporated into Influenza Virus Particles Inhibits Gamma Interferon Signaling and Promotes Viral Replication

Berri

Haffar

Lê

et al. 2014

J Virol

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“…Anionic phospholipids, including PS, have been implicated as receptors and cofactors for several viruses, including VSV, rhabdoviruses, hepatitis B, influenza viruses, hemorrhagic septicemia, Sendai virus, rubella virus, and Sindbus virus (33)(34)(35)(36)(37)(38)(39)(40). Characterization of lipid composition of HIV-1 envelope shows that many lipids, including glycosphingolipids, cholesterol, and PS, are found in the membrane at a higher frequency than what is represented in the host membrane, suggesting a selective incorporation of these lipids (14).…”

Section: Discussionmentioning

confidence: 99%

Phosphatidylserine on HIV Envelope Is a Cofactor for Infection of Monocytic Cells

Callahan¹,

Popernack

Tsutsui³

et al. 2003

The Journal of Immunology

125

116

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HIV-1 is an enveloped retrovirus that acquires its outer membrane as the virion exits the cell. Because of the association of apoptosis with the progression of AIDS, HIV-1-infected T cells or macrophages might be expected to express elevated levels of surface phosphatidylserine (PS), a hallmark of programmed cell death. Virions produced by these cells would also be predicted to have PS on the surface of their envelopes. In this study, data are presented that support this hypothesis and suggest that PS is required for macrophage infection. The PS-specific protein annexin V was used to enrich for virus particles and to inhibit HIV-1 replication in primary macrophages, but not T cells. HIV-1 replication was also significantly inhibited with vesicles consisting of PS, but not phosphatidylcholine. PS is specifically required for HIV-1 infection because viruses pseudotyped with vesicular stomatitis virus G and amphotropic murine leukemia virus envelopes were not inhibited by PS vesicles or annexin V. These data indicate that PS is an important cofactor for HIV-1 infection of macrophages.

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“…Subsequently, it was reported that Annexin V aids in the entry of influenza virus and that annexins may serve as a receptor for the viruses (Huang et al, 1996). However, different annexins have different impact on influenza virus replication.…”

Section: A) Annexins and Influenza Infectionmentioning

confidence: 99%

DAMPs and influenza virus infection in ageing

Samy

Lim

2015

Ageing Research Reviews

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Involvement of annexin V in the entry of influenza viruses and role of phospholipids in infection

Cited by 42 publications

References 21 publications

Annexin V Incorporated into Influenza Virus Particles Inhibits Gamma Interferon Signaling and Promotes Viral Replication

Annexin V Incorporated into Influenza Virus Particles Inhibits Gamma Interferon Signaling and Promotes Viral Replication

Phosphatidylserine on HIV Envelope Is a Cofactor for Infection of Monocytic Cells

DAMPs and influenza virus infection in ageing

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