Abstract
The innate immune system provides a frontline defense against viral infection by limiting viral replication and alerting the adaptive immune response to the presence of danger. Various receptors recognize patterns characteristic of invading pathogens and induce the production of type-1 interferons that mediate a broad range of immune responses. The current issue of Viral Immunology features two reviews that focus on the innate response to two important human pathogens: herpes simplex virus type 1 (HSV-1) and the human papillomavirus (HPV).
HSV-1, which primarily causes oral herpes (cold sores), establishes lifelong latency in neurons and can reactivate repeatedly throughout the life of host. Although viral reactivation induces a rapid innate immune response, a number of viral evasion mechanisms allow the virus to replicate extensively until the adaptive immune response can control the infection. Substantial progress has been made in our understanding innate pathogen recognition and its evasion. Here, Amin et al. review the host's antiviral defense machinery and the evasion mechanisms employed by HSV-1 to establish infection.
One important pathogen-sensing molecule is Toll-like receptor 4 (TLR4), which recognizes and binds to several different bacterial and viral-associated molecules. It has been hypothesized that TLR4 may play a key role in HPV infection and its related complications. In a review article, Bahramabadi and colleagues discuss recent advances in our understanding of the role of TLR4 in both HPV control by the innate immune system and its cancer-related pathogenesis.
Three additional articles in this issue of Viral Immunology address other aspects of the innate response to viral infection. Malik and colleagues note that CD81 serves as immune-modulator, playing a role in the growth and metastasis of hepatitis C virus (HCV)-mediated hepatocellular carcinoma. The molecule also serves as a coreceptor of viral entry and is enriched in exosomes. The authors show that CD81-positive exosomes carry HCV particles, and this association plays a pivotal role in establishing persistent infection, thus leading to hepatocellular carcinoma progression. The authors speculate that exosomal CD81 might be a prognostic marker and therapeutic target for HCV infection. Ninla-aesong and colleagues have evaluated the expression of cytokines, chemokines, and matrix-metalloproteinases in patients with persistent arthritis caused by a prior chikungunya virus infection. Their data indicate that there are increased levels of proinflammatory markers in patients with severe pain, compared with patients with nonsevere pain, suggesting that they play a role in disease severity. The authors suggest that the levels of proinflammatory cytokines and chemokines may serve as biomarkers for persistent arthralgia and severe disease.
Finally, Bhaskaran et al. report on an association between the HLA-A, B, DRB, and DQB alleles and persistent HPV-16 infection in women from Tamil Nadu, India.
I thank all of the authors for their excellent contributions and all of the reviewers who have worked to ensure the high quality of articles accepted for publication.