Herpes Simplex Virus and the Chemokines That Mediate the Inflammation

Abstract

Herpes simplex viruses (HSV) are highly pervasive pathogens in the human host with a seroconversion rate upwards of 60% worldwide. HSV type 1 (HSV-1) is associated with the disease, herpetic stromal keratitis, the leading cause of infectious corneal blindness in the industrialized world. Individuals suffering from genital herpes associated with HSV type 2 (HSV-2) are found to be two to three fold more susceptible in acquiring human immunodeficiency virus (HIV). The morbidity associated with these infections is principally due to the inflammatory response, the development of lesions, and scarring. Chemokines have become an important aspect in understanding the host immune response to microbial pathogens due in part to the timing of expression. In this paper, we will explore the current understanding of chemokine production as it relates to the orchestration of the immune response to HSV infection.

CD4+ T cell migration into the cornea is reduced in CXCL9 deficient but not CXCL10 deficient mice following herpes simplex virus type 1 infection

“…Both resident corneal cells and infiltrating leukocytes generate the chemokines detected in the present study including CXCL9 and CXCL10 [11,[34][35][36][37]. Out of the six chemokines investigated, only CCL2 levels were associated with sensitivity to infection since CXCL10−/ − mice possessed significantly more virus and expressed elevated levels of CCL2 in the cornea in comparison to the less sensitive WT or CXCL9−/− mice.…”

“…Likewise, IL-1β, IL-6, and TNF-α levels were not detectable or were significantly lower in the cornea of CXCL9−/− mice compared to the other two groups ( Table 1). The expression of these cytokines/chemokines is in response to infection since uninfected mouse corneas contain significantly lower levels of the assayed analytes [11].…”

“…Th2 cytokines exacerbate HSV-1 infection whereas Th1 cytokines are principally produced by those cells infiltrating the infected tissue and contribute towards resistance to virus replication and spread [8][9][10]. Chemokines expressed locally are likely involved in the recruitment of leukocytes into the site of infection with CCL2 and CXCL10 expressed or up-regulated significantly within the first 36 hr post infection relative to other chemokines including CCL3, CCL5, CXCL1, and CXCL9 [11].…”

Regulation of CXCL-8 (Interleukin-8) Induction by Double-Stranded RNA Signaling Pathways during Hepatitis C Virus Infection

“…Indeed, inductions of inflammatory cytokines and chemokines such as CXCL-6, CXCL-8, and TNF-␣ have been reported in patients with chronic hepatitis C (11,13,18,39,51). In this case, the inflammatory response may do more harm than good because deregulation of inflammatory cytokines and chemokines creates an environment within the liver that is harsh and leads to hepatocyte turnover and regeneration (7,17,35,37,57). It has been suggested that chronic inflammation is mechanistically involved in the establishment of cancer (41), in particular hepatocellular carcinoma (5), so a deregulated inflammatory response may also have severe pathological sequelae.…”

Viral vectors for in vivo gene transfer in Parkinson's disease: Properties and clinical grade production

“…The wild type virus is the pathogen that is associated with cold sores, corneal blindness, and encephalitis (Carr and Tomanek, 2006). Wt-HSV can infect a wide variety of cells due to the envelope binding to heparan sulfate and herpes virus entry mediators.…”