ID: 52: Interferon-位 controls the spread of influenza viruses from the upper respiratory tract to the lungs and restricts virus transmission in mice

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• 作者：Jonas Klinkhammer¹ ; ² ; ; Daniel Schnepf¹ ; Marilena Schwaderlapp¹ ; Tanel Mahlakõ ; iv¹ ; Peter Staeheli¹
• 刊名：Cytokine
• 出版年：2015
• 出版时间：November 2015
• 年：2015
• 卷：76
• 期：1
• 页码：74
• 全文大小：41 K

文摘

Previous infection studies have invariably assigned a minor role to interferon-位$\mathrm{位}$ (IFN-位$\mathrm{位}$) in the control of influenza viruses in the lungs of mice. However, when we administered the virus selectively to the upper respiratory tract, we came to a completely different conclusion. Under such more physiological conditions, influenza virus replication was largely restricted to the nasal tissue in wild-type mice. In contrast, in mice lacking functional receptors for IFN-位$\mathrm{位}$, influenza virus was frequently observed to spread to the lungs. Interestingly, the virus spread more frequently to the lungs in mice lacking functional receptors for IFN-位$\mathrm{位}$ than in mice lacking functional receptors for IFN-伪$\mathrm{伪}$/94592d5314b422ecaf" title="Click to view the MathML source">尾$\mathrm{尾}$, indicating that IFN-位$\mathrm{位}$ is more critical for virus restriction in the upper respiratory tract.

We further observed that the Udorn (H3N2) influenza A virus strain is readily transmitted upon contact among mice lacking functional receptors for both IFN-伪$\mathrm{伪}$/94592d5314b422ecaf" title="Click to view the MathML source">尾$\mathrm{尾}$ and IFN-位$\mathrm{位}$. Contact transmission of this virus was also efficient when mice lacking functional receptors for IFN-位$\mathrm{位}$ were employed. In contrast, wild-type mice and mice lacking functional receptors for IFN-伪$\mathrm{伪}$/94592d5314b422ecaf" title="Click to view the MathML source">尾$\mathrm{尾}$ transmitted the virus only with reduced efficacy. These findings demonstrate that the crucial role of IFN-位$\mathrm{位}$ in influenza virus restriction is only getting apparent under experimental conditions which imitate the physiological route of virus infection.