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The Complex Role of STAT3 in Viral Infections.

Kuchipudi SV - J Immunol Res (2015)

Bottom Line: Several studies reported differential regulation of STAT3 in a range of viral infections.Interestingly, STAT3 appears to direct seemingly contradictory responses and both pro- and antiviral roles of STAT3 have been described.Some of the key unanswered questions and the gap in our current understanding of the role of STAT3 in viral pathogenesis are discussed.

View Article: PubMed Central - PubMed

Affiliation: School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington LE12 5RD, UK.

ABSTRACT
Signal transducer and activators of transcription-3 (STAT3) regulates diverse biological functions including cell growth, differentiation, and apoptosis. In addition, STAT3 plays a key role in regulating host immune and inflammatory responses and in the pathogenesis of many cancers. Several studies reported differential regulation of STAT3 in a range of viral infections. Interestingly, STAT3 appears to direct seemingly contradictory responses and both pro- and antiviral roles of STAT3 have been described. This review summarized the currently known functions of STAT3 in the regulation of viral replication and pathogenesis of viral infections. Some of the key unanswered questions and the gap in our current understanding of the role of STAT3 in viral pathogenesis are discussed.

No MeSH data available.


Related in: MedlinePlus

STAT3 regulation in viral infections. Epstein-Barr virus (EBV) oncoprotein latent membrane protein 1 (LMP1), human immunodeficiency virus type 1 (HIV-1) Nef protein, hepatitis C virus (HCV) core protein, HCV nonstructural protein 5A (NS5A), hepatitis B virus X protein (HBx), Kaposi's sarcoma-associated herpesvirus (KSHV), saimiri transforming protein (STP) oncogene of Herpesvirus saimiri subgroup A strain 11 (STP-A11), and Varicella-zoster virus (VZV) activate STAT3 phosphorylation. Influenza A virus (IAV) nonstructural protein 1 (NS-1) human metapneumovirus (hMPV) and human cytomegalovirus (HCMV) inhibit STAT3 phosphorylation. Severe acute respiratory syndrome coronavirus (SARS-CoV) infection results in STAT3 dephosphorylation.
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fig3: STAT3 regulation in viral infections. Epstein-Barr virus (EBV) oncoprotein latent membrane protein 1 (LMP1), human immunodeficiency virus type 1 (HIV-1) Nef protein, hepatitis C virus (HCV) core protein, HCV nonstructural protein 5A (NS5A), hepatitis B virus X protein (HBx), Kaposi's sarcoma-associated herpesvirus (KSHV), saimiri transforming protein (STP) oncogene of Herpesvirus saimiri subgroup A strain 11 (STP-A11), and Varicella-zoster virus (VZV) activate STAT3 phosphorylation. Influenza A virus (IAV) nonstructural protein 1 (NS-1) human metapneumovirus (hMPV) and human cytomegalovirus (HCMV) inhibit STAT3 phosphorylation. Severe acute respiratory syndrome coronavirus (SARS-CoV) infection results in STAT3 dephosphorylation.

Mentions: STAT3 is either positively or negatively regulated in a range of viral infections depending on the type of virus involved. Figure 3 provides a summary of positive or negative regulation of STAT3 by viruses. A number of viral proteins interact with STAT3 resulting in the phosphorylation activation. Epstein-Barr virus (EBV) oncoprotein latent membrane protein 1 (LMP1) [67], human immunodeficiency virus type 1 (HIV-1) Nef protein [68], hepatitis C virus (HCV) core protein [69], HCV nonstructural protein 5A (NS5A) [70], mitochondrially associated hepatitis B virus X protein (HBx) [71], Kaposi's sarcoma-associated herpesvirus (KSHV) [72], saimiri transforming protein (STP) oncogene of Herpesvirus saimiri subgroup A strain 11 (STP-A11) [73], and Varicella-zoster virus (VZV) [74] promote STAT3 phosphorylation in infected cells.


The Complex Role of STAT3 in Viral Infections.

Kuchipudi SV - J Immunol Res (2015)

STAT3 regulation in viral infections. Epstein-Barr virus (EBV) oncoprotein latent membrane protein 1 (LMP1), human immunodeficiency virus type 1 (HIV-1) Nef protein, hepatitis C virus (HCV) core protein, HCV nonstructural protein 5A (NS5A), hepatitis B virus X protein (HBx), Kaposi's sarcoma-associated herpesvirus (KSHV), saimiri transforming protein (STP) oncogene of Herpesvirus saimiri subgroup A strain 11 (STP-A11), and Varicella-zoster virus (VZV) activate STAT3 phosphorylation. Influenza A virus (IAV) nonstructural protein 1 (NS-1) human metapneumovirus (hMPV) and human cytomegalovirus (HCMV) inhibit STAT3 phosphorylation. Severe acute respiratory syndrome coronavirus (SARS-CoV) infection results in STAT3 dephosphorylation.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4496485&req=5

fig3: STAT3 regulation in viral infections. Epstein-Barr virus (EBV) oncoprotein latent membrane protein 1 (LMP1), human immunodeficiency virus type 1 (HIV-1) Nef protein, hepatitis C virus (HCV) core protein, HCV nonstructural protein 5A (NS5A), hepatitis B virus X protein (HBx), Kaposi's sarcoma-associated herpesvirus (KSHV), saimiri transforming protein (STP) oncogene of Herpesvirus saimiri subgroup A strain 11 (STP-A11), and Varicella-zoster virus (VZV) activate STAT3 phosphorylation. Influenza A virus (IAV) nonstructural protein 1 (NS-1) human metapneumovirus (hMPV) and human cytomegalovirus (HCMV) inhibit STAT3 phosphorylation. Severe acute respiratory syndrome coronavirus (SARS-CoV) infection results in STAT3 dephosphorylation.
Mentions: STAT3 is either positively or negatively regulated in a range of viral infections depending on the type of virus involved. Figure 3 provides a summary of positive or negative regulation of STAT3 by viruses. A number of viral proteins interact with STAT3 resulting in the phosphorylation activation. Epstein-Barr virus (EBV) oncoprotein latent membrane protein 1 (LMP1) [67], human immunodeficiency virus type 1 (HIV-1) Nef protein [68], hepatitis C virus (HCV) core protein [69], HCV nonstructural protein 5A (NS5A) [70], mitochondrially associated hepatitis B virus X protein (HBx) [71], Kaposi's sarcoma-associated herpesvirus (KSHV) [72], saimiri transforming protein (STP) oncogene of Herpesvirus saimiri subgroup A strain 11 (STP-A11) [73], and Varicella-zoster virus (VZV) [74] promote STAT3 phosphorylation in infected cells.

Bottom Line: Several studies reported differential regulation of STAT3 in a range of viral infections.Interestingly, STAT3 appears to direct seemingly contradictory responses and both pro- and antiviral roles of STAT3 have been described.Some of the key unanswered questions and the gap in our current understanding of the role of STAT3 in viral pathogenesis are discussed.

View Article: PubMed Central - PubMed

Affiliation: School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington LE12 5RD, UK.

ABSTRACT
Signal transducer and activators of transcription-3 (STAT3) regulates diverse biological functions including cell growth, differentiation, and apoptosis. In addition, STAT3 plays a key role in regulating host immune and inflammatory responses and in the pathogenesis of many cancers. Several studies reported differential regulation of STAT3 in a range of viral infections. Interestingly, STAT3 appears to direct seemingly contradictory responses and both pro- and antiviral roles of STAT3 have been described. This review summarized the currently known functions of STAT3 in the regulation of viral replication and pathogenesis of viral infections. Some of the key unanswered questions and the gap in our current understanding of the role of STAT3 in viral pathogenesis are discussed.

No MeSH data available.


Related in: MedlinePlus