Interferon-Inducible Mx Gene Expression in Cotton Rats: Cloning, Characterization, and Expression During Influenza Viral Infection

2006 ◽  
Vol 26 (12) ◽  
pp. 914-921 ◽  
Author(s):  
Lioubov M. Pletneva ◽  
Otto Haller ◽  
David D. Porter ◽  
Gregory A. Prince ◽  
Jorge C.G. Blanco
Author(s):  
Lei Zhang ◽  
Youwei Zhang

Coronavirus disease 2019 (COVID-19) is caused by infection with the 2019 novel coronavirus 2 (2019-nCoV, now referred to as SARS-CoV-2). COVID-19 has become a global pandemic since its outbreak at the end of Dec 2019. COVID-19 could lead to severe acute respiratory disease, especially to those who have reduced immunity. Binding of the viral Spike protein (S) to its receptor ACE2 (Angiotensin Converting Enzyme 2) on the surface of target cells has been proven to be key for virus entry and infection. Although ACE2 expression in the respiratory system is necessary for pneumonia infection by SARS-CoV-2, the regulation of ACE2 gene expression remains poorly investigated, especially for patients that are in pre-pathological conditions. Here, by analyzing The Gene Expression Omnibus (GEO) database, we investigated the expression regulation of ACE2 in various kinds of primary epithelial cells from the respiratory system after influenza A or respiratory Syncytial Virus (RSV) infection. Our analyses reveal that infection of influenza A, RSV or influenza vaccines greatly increased ACE2 expression, suggesting that influenza viral infection could represent a high risk factor for developing COVID-19. We also found that the regulatory effect of influenza A virus on ACE2 expression is associated with activation of the interferon beta-induced pathway and viral RNA-activated host response. Together, our data provide a theoretical framework for clinical classification for SARS-CoV-2 infection susceptibility and could be used for future prevention and therapy treatment for COVID-19.


Author(s):  
Rabih Halwani ◽  
Mehrnoosh Doroudchi ◽  
Mohamed El-Far ◽  
Andre Tanel ◽  
Yu Shi ◽  
...  

1991 ◽  
Vol 116 (1-4) ◽  
pp. 261-265 ◽  
Author(s):  
T. M. Chambers ◽  
Virginia S. Hinshaw ◽  
Y. Kawaoka ◽  
B. C. Easterday ◽  
R. G. Webster

2018 ◽  
Vol 7 (2) ◽  
pp. 50-55
Author(s):  
Li Han

AbstractThe harms of seasonal flu and global pandemic influenza have generally attracted attention. However, the currently administered influenza drugs and flu vaccines have certain limitations. Since the discovery of the small interfering RNA (siRNA) and its mediated RNA interference process, this molecule has been widely used in the study of anti-influenza viral infections because of its high specificity and strong selectivity. The results provided new concepts for the prevention and treatment of influenza virus. However, the siRNA still faces an enormous challenge despite extensive studies on this molecule. The research progress of siRNA in anti-influenza viral infection was reviewed in this study.


2021 ◽  
Author(s):  
Phillip J Dexheimer ◽  
Mario Pujato ◽  
Krishna Roskin ◽  
Matthew T Weirauch

AbstractMotivationHuman viruses cause significant mortality, morbidity, and economic disruption worldwide. The human gene expression response to viral infection can yield important insights into the detrimental effects to the host. To date, hundreds of studies have performed genome-scale profiling of the effect of viral infection on human gene expression. However, no resource exists that aggregates human expression results across multiple studies, viruses, and tissue types.ResultsWe developed the Virus Expression Database (VExD), a comprehensive curated resource of transcriptomic studies of viral infection in human cells. We have processed all studies within VExD in a uniform manner, allowing users to easily compare human gene expression changes across conditions.Availability and ImplementationVExD is freely accessible at https://vexd.cchmc.org for all modern web browsers. An Application Programming Interface (API) for VExD is also available. The source code is available at https://github.com/pdexheimer/[email protected], [email protected]


Blood ◽  
1997 ◽  
Vol 90 (3) ◽  
pp. 1186-1191 ◽  
Author(s):  
Marcelo G. Horenstein ◽  
Roland G. Nador ◽  
Amy Chadburn ◽  
Elizabeth M. Hyjek ◽  
Giorgio Inghirami ◽  
...  

Primary effusion (body cavity–based) lymphoma (PEL) is a recently recognized subtype of malignant lymphoma that exhibits distinctive clinical and biological features, most notably its usual infection with the Kaposi's sarcoma–associated herpesvirus (KSHV). The vast majority of cases also contain Epstein-Barr virus (EBV). This dual viral infection is the first example of a consistent dual herpesviral infection in a human neoplasm and provides a unique model to study viral interactions. We analyzed the pattern of EBV latent gene expression to determine the pathogenic role of this agent in PELs. We examined five PELs coinfected with EBV and KSHV by reverse transcription-polymerase chain reaction (RT-PCR), in situ hybridization, and immunohistochemistry. EBER1 mRNA, a consistent marker of viral latency, was positive in all PEL cases, although at lower levels than in the non-PEL controls due to EBER1 expression by only a variable subset of lymphoma cells. Qp-initiated mRNA, encoding only EBNA1 and characteristic of latencies I and II, was positive in all PEL cases. Wp- and Cp-initiated mRNAs, encoding all EBNAs and characteristic of latency III, were negative in all cases. LMP1 mRNA, expressed in latencies II and III, was present in three cases of PEL, although at very low levels that were not detectable at the protein level by immunohistochemistry. Low levels of LMP2A mRNA were detected in all cases. BZLF1, an early-intermediate lytic phase marker, was weakly positive in four cases, suggesting a productive viral infection in a very small proportion of cells, which was confirmed by ZEBRA antigen expression. Therefore, PELs exhibit a restricted latency pattern, with expression of EBNA1 in all cases, and low LMP1 and LMP2A levels.


2011 ◽  
Vol 59 (8) ◽  
pp. 3730-3737 ◽  
Author(s):  
Rong-Rong He ◽  
Min Wang ◽  
Cong-Zhi Wang ◽  
Bang-Tian Chen ◽  
Chun-Ni Lu ◽  
...  

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