Abstract
The neonate (NB) is susceptible to disseminated HSV. To investigate the role of IFNγ and TNFα, two cytokines potentially important in defense against HSV dissemination, we studied 23 HSV infected (HSV+) NB, 11 uninfected (HSV-) NB and 8 adults (AD) with primary HSV infection. We evaluated MC thymidine uptake (thy) and IFNy production after ConA or HSV stimulation.
HSV stimulated thy and IFNγ response increased with time in HSV + NB but much more slowly than the AD response. By 28d all AD, but only 3/12 NB, had SI >3 and IFNγ >10 to HSV. HSV- NB did not respond. ConA stimulated minimal amounts of IFNγ in all NB. Production of activity cytolytic for L-929 cells, which was >80% neutralized by antibody to TNFα, by HSV stimulated NB MC correlated with IFNγ. 6/6 NB with IFNγ >10 and 1/6 NB with IFNγ <10 produced TNFα >10 U/ml. NB concomitantly develop the ability to produce HSV stimulated IFNγ and TNFα. Delayed production of IFNγ and perhaps TNF by HSV+ NB may partly explain the difference in severity of infection compared to the AD.
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Burchett, S., Mohan, K., Corey, L. et al. DELAYED PRODUCTION OF INTERFERON-GAMMA (IFNγ) AND TUMOR NECROSIS FACTOR (TNFα) BY MONONUCLEAR CELLS (MC) OF HERPES SIMPLEX VIRUS (HSV) INFECTED NEONATES (NB). Pediatr Res 21 (Suppl 4), 309 (1987). https://doi.org/10.1203/00006450-198704010-00851
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DOI: https://doi.org/10.1203/00006450-198704010-00851