Scientists identify new class of immune cells that suppress genital herpes

Scientists identify new class of immune cells that suppress genital herpes

In an effort to determine the influence of viral pathogens in declining coral health, researchers at San Diego State University recently used metagenomic analysis with the Genome Sequencer System from 454 Life Sciences to sequence Porites compressa coral samples under varying environmental stressors. Recently, an x-ray structure of the nearly full-length trimeric gB ectodomain was determined. The discovery of this subtype of immune cells, called CD8αα+ T cells, opens a new avenue of research to develop a vaccine to prevent and treat herpes simplex virus type 2, or HSV-2. The latter approach selected ligands with homology to residues 171 to 176 of UL42. On the basis of biochemical fractionation of infected cells, UL24 appeared to be predominantly nucleus associated, especially at later times in infection. Interestingly, ASYMP individuals had a significantly higher proportion of CD45RAlowCCR7lowCD44highCD62LlowCD27lowCD28lowCD8+ effector memory CD8+ T cells (TEMs) specific to the three epitopes, compared with symptomatic individuals (with a history of numerous episodes of recurrent ocular herpetic disease). It was found that mutations in both the N- and C-terminal halves of ICP22 result in similar defects in viral late gene expression and growth in HEL cells, despite having distinctly different effects on Pol II.

Scientists identify new class of immune cells that suppress genital herpes
Finally, several HSV-1 factors were also found to be associated with Rep, including UL12. These results identify a conserved domain of gL that is critical for its binding to gH and two noncontiguous regions of gL, one of which contains the conserved domain, that are critical for the gH/gL complex to perform its role in membrane fusion. It has been assumed that peptides A, E, and G exert their inhibitory activity by binding to UL42 and thus that the H1228A and R1229A substitutions prevent binding to UL42. Previous research by the same research group showed that the nerve endings reach the dermal-epidermal junction and release the virus that infects the skin and can cause lesions. Prior to this research, CD8αα+ T cells were known to exist in the gut mucosa. Much of the research on CD8+ T cells has focused on studying them in the circulating blood, which has a dominant phenotype of CD8αβ+. Fred Hutch and UW scientists compared the two types of CD8+ T cells and found that only the CD8αα+ T cells persist in the skin while CD8αβ+ T cells diminished from the tissue after healing of a herpes lesion.

The research involved using novel technologies to examine the T cells in human tissues. In all, the work provides a roadmap that can be applied to other human diseases, according to Zhu. Zhu said the studies the research group performed in humans are unique. “To our knowledge, we are the only research group to use sequential human biopsies to study CD8+ T cell function in situ, in their natural spatial distribution and at their original physiological state,” she said. According to the federal Centers for Disease Control and Prevention, 776,000 people in the United States are newly infected with herpes annually. Nationwide, 16.2 percent, or about one out of six people aged 14 to 49 years have genital HSV-2 infection. Generally, a person can only get HSV-2 infection during sexual contact with someone who has a genital HSV-2 infection.

It has been proposed that certain regions in gH might function as a fusion peptide and as heptad repeats that fold up into six-helix bundles (6–8). Most individuals infected with HSV-2 or the related HSV-1, which causes genital herpes and cold sores, experience either no symptoms or have very mild symptoms that go unnoticed or are mistaken for another skin condition. However, in these cases, binding was not shown to be specific to both binding partners, for example, by examining control or mutant proteins.

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