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Blood, 15 April 2001, Vol. 97, No. 8, pp. 2366-2373
IMMUNOBIOLOGY
Primary human herpesvirus 8 infection generates a broadly
specific CD8+ T-cell response to viral lytic
cycle proteins
Qiong J. Wang,
Frank J. Jenkins,
Lisa P. Jacobson,
Lawrence A. Kingsley,
Richard D. Day,
Zhi-Wei Zhang,
Yuan-Xiang Meng,
Philip E. Pellet,
Konstantin G. Kousoulas,
Abolghasem Baghian, and
Charles R. Rinaldo Jr
From the Department of Infectious Diseases and
Microbiology and the Department of Biostatistics, Graduate School of
Public Health, and the Department of Pathology, School of Medicine,
University of Pittsburgh, Pittsburgh, Pennsylvania; Department of
Epidemiology, The Johns Hopkins University, Baltimore, Maryland;
Centers for Disease Control and Prevention, Atlanta, Georgia; and
School of Veterinary Medicine, Louisiana State University, Baton Rouge,
Louisiana.
Human herpesvirus 8 (HHV-8) is a recently discovered
gammaherpesvirus that is the etiologic agent of Kaposi sarcoma (KS). The natural history of primary HHV-8 infection, including clinical outcome and host immune responses that may be important in preventing disease related to HHV-8, has not been elucidated. The present study
characterized the clinical, immunologic, and virologic parameters of
primary HHV-8 infection in 5 cases detected during a 15-year longitudinal study of 108 human immunodeficiency virus type 1 seronegative men in the Multicenter AIDS Cohort Study. Primary HHV-8
infection was associated with mild, nonspecific signs and symptoms of
diarrhea, fatigue, localized rash, and lymphadenopathy. There were no
alterations in numbers of CD4+ or CD8+ T cells
or CD8+ T-cell interferon  (IFN-) production to
mitogen or nominal antigen. CD8+ cytotoxic T-lymphocyte
precursor (CTLp) and IFN- reactivity were detected during primary
HHV-8 infection, with broad specificity to 5 lytic cycle proteins of
HHV-8 encoded by open reading frame 8 (ORF 8; glycoprotein B homolog of
Epstein-Barr virus), ORF 22 (gH homolog), ORF 25 (major capsid protein
homolog), ORF 26 (a minor capsid protein homolog), or ORF 57 (an early
protein homolog), in association with increases in serum antibody
titers and appearance of HHV-8 DNA in blood mononuclear cells.
CD8+ T-cell responses to HHV-8 decreased by 2 to 3 years
after primary infection. This antiviral T-cell response may control
initial HHV-8 infection and prevent development of disease.
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