Research Paper Herpes Simplex

GEN-003 is a candidate therapeutic vaccine containing HSV-2 g D2∆TMR and ICP4.2, and Matrix-M2 adjuvant.

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But how viruses emerge from this sanctuary has been poorly understood, in part because it’s difficult to study ganglion cells in isolation.

“The ganglion is like a miniature organ,” explains Dr. “It contains many different types of cells, including immune cells.” The researchers’ solution was an innovative culturing technique “made of nothing but neurons,” says Dr. “It allows us to study the molecular signaling and circuitry in depth, without interference from other cells.” With a clear window onto the infected cells, the researchers made a startling discovery: when jostled awake by stress, HSV-1 bursts into action, releasing a flood of proteins that jams the host’s immune reaction to interferon signals from infected cells, effectively disarming the cells’ alarm system.

We recruited healthy, HSV-2–seropositive adults 18–50 years of age with a history of recurrent genital herpes for at least 1 year and 3–9 recurrences per year in the absence of antiviral suppressive therapy.

HSV-2 infection was documented by Western blot, HSV-2 Herpe Select 2 immunoglobulin G (Ig G)–specific enzyme-linked immunosorbent assay (ELISA; an index value of 3.5 indicates a positive result), HSV-2 Ig G Liaison assay, or type-specific culture or polymerase chain reaction (PCR), and findings were confirmed for all participants during screening by HSV-2 Ig G Liaison assay.

The management of genital herpes currently includes episodic or daily suppressive therapy with nucleoside analogues, which abrogates most recurrences but only partly reduces viral shedding and transmission [1, 2].

GEN-003 contains a transmembrane deletion mutant of glycoprotein D (g D2ΔTMR), a primary target antigen for neutralizing antibody and T cells, combined with a large fragment of infected cell protein 4 (ICP4.2), an HSV-2 T-cell antigen prioritized through human T-cell screens.

“This happens in the very first instant that HSV-1 reactivates,” explains Angus C.

Wilson, Ph D, an associate professor of microbiology and another of the paper’s coauthors.

As with all herpes virus infections, HSV-1 infections are cureless and lifelong.

The virus burrows into the nervous system, nesting deep inside the base of the brain, in an area of nerve cells called the trigeminal ganglion.