# The regulatory roles of STAT3 protein in the pathogenesis of viral infections

## TL;DR

This paper reviews how the STAT3 protein influences viral infections by regulating immune responses and viral replication.

## Contribution

The paper provides a comprehensive review of recent findings on STAT3's role in host-virus interactions and antiviral immunity.

## Key findings

- STAT3 phosphorylation inhibits viral invasion but can be exploited by viruses to evade immune detection.
- Excessive STAT3 activation promotes viral replication and persistence.
- The exact mechanisms of STAT3 in viral pathogenesis remain unclear and require further study.

## Abstract

Signal transducer and activator of transcription 3 (STAT3) serves as a critical regulatory molecule in a multitude of physiological processes, encompassing cell proliferation, differentiation, immune defense, and inflammatory responses. The interaction between STAT3 and viruses is highly intricate, with particular relevance to the viral life cycle. It is widely acknowledged that during viral infection, the phosphorylation of STAT3, which is triggered by upstream activators such as interleukin-6 (IL-6), can exert an effective inhibitory effect on viral invasion. However, accumulating evidence has demonstrated that viruses may exploit their interaction with STAT3 to evade host immune surveillance, thereby facilitating viral persistence. Furthermore, the excessive activation of STAT3 induced by viral infection directly promotes viral replication. The precise mechanism underlying the role of STAT3 in viral infection and pathogenicity remains to be further elucidated. In this review, we summarize recent findings regarding the critical roles of STAT3 in host-virus interactions. Additionally, we discuss the mechanisms of related molecules involved in the antiviral immune response.