Abstract
Antiviral restriction factors are host cellular proteins that constitute a first line of defense blocking viral replication and propagation. In addition to interfering at critical steps of the viral replication cycle, some restriction factors also act as innate sensors triggering innate responses against infections. Accumulating evidence suggests an additional role for restriction factors in promoting antiviral cellular immunity to combat viruses. Here, we review the recent progress in our understanding on how restriction factors, particularly APOBEC3G, SAMHD1, Tetherin, and TRIM5α have the cell-autonomous potential to induce cellular resistance against HIV-1 while promoting antiviral innate and adaptive immune responses. Also, we provide an overview of how these restriction factors may connect with protein degradation pathways to modulate anti-HIV-1 cellular immune responses, and we summarize the potential of restriction factors-based therapeutics. This review brings a global perspective on the influence of restrictions factors in intrinsic, innate, and also adaptive antiviral immunity opening up novel research avenues for therapeutic strategies in the fields of drug discovery, gene therapy, and vaccines to control viral infections.
Highlights
Restriction factors are host cellular proteins contributing to the frontline defense against viral infections
Our results strongly indicate that non-human TRIM5α variants play a role in restriction and increase cytotoxic T lymphocytes (CTLs) activation linking innate and adaptive immune responses in Human Immunodeficiency Virus type 1 (HIV-1) infection
Cellular host restriction factors including APOBEC3G, Tetherin, SAMHD1, and TRIM5α constitute a first barrier of the intrinsic cellular response against HIV-1 and other viral infections
Summary
Restriction factors are host cellular proteins contributing to the frontline defense against viral infections. Restriction factors recognize and interfere with specific steps of the replication cycle of viruses, thereby blocking infection. They are generally interferon (IFN)-inducible and their inherent features, such as constitutive expression in different cell types, self-sufficient activity, and rapidity of action, confer a potent and early restriction of viruses [1]. The continuous adaptation of HIV-1 to the pressure exerted by the antiviral activities of restriction factors underscores the importance of restriction factors in controlling viral infections. During the acute phase of viral infections, pro-inflammatory cytokine storms contribute
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