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Humoral immune response to HSV‐1 and HSV‐2 viral proteins in patients with primary genital herpes
Author(s) -
Ashley Rhoda,
Benedetti Jacqueline,
Corey Lawrence
Publication year - 1985
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.1890170208
Subject(s) - seroconversion , virology , antibody , immune system , immunology , hsl and hsv , glycoprotein , biology , herpesviridae , medicine , viral disease , virus , microbiology and biotechnology
The humoral immune response to HSV‐1 and HSV‐2 proteins was examined in patients with primary first‐episode genital herpes. Ten patients had culture‐proven HSV‐1 infections, 37 had HSV‐2 infections, and all were seronegative to HSV proteins before developing their infections. Development of serum antibodies to individual HSV proteins and glycoproteins was determined by immunoprecipitation of radiolabeled HSV‐1‐ and HSV‐2‐ infected cell proteins and subsequent gel electrophoresis. In HSV‐1 patients, a sequential development of antibodies to HSV‐1 proteins was observed with early appearance of antibodies to the nucleocapsid protein p148 and to glycoproteins gB and gC. Seroconversion to gD and to a polypeptide of 88,000 molecular weight (p88) occurred next, and, finally, seroconversion to gE and to a nonglycosylated 66,000 dalton protein p66. In HSV‐2 patients, antibodies to HSV‐2 proteins p148, gB, and p88 appeared within 1 week of onset of symptoms. Seroconversion to p66, gD, and to a complex of glycoproteins gC and gE (g80) occurred later, at a mean time of approximately 3 weeks. Seroconversion to HSV‐1 gB, p88, and p66 occurred significantly later than seroconversion to the homologous counterparts. Seroconversion within 21 days of onset to HSV‐2 gD, g80, and p66 was associated with a longer time to the first recurrence in HSV‐2 patients, suggesting a possible role of these antibodies, alone or in combination, in the maintenance of HSV‐2 latency in humans.