Hsia J, Sztein M B, Naylor P H, Simon G L, Goldstein A L, Hayden F G
Department of Medicine, George Washington University School of Medicine and Health Sciences, Washington, DC.
Lymphokine Res. 1989 Winter;8(4):383-91.
Cellular immune response to localized upper respiratory viral infection was studied in two groups of healthy volunteers infected with an unnumbered rhinovirus serotype (Hanks). In the first group of 18 volunteers, serum levels of thymosin alpha 1 rose on day 5 following rhinovirus challenge. This observation was confirmed in a second group of 20 normal volunteers inoculated with the same rhinovirus strain; there was a slight increase in thymosin alpha 1 levels on day 3 and a significant rise on day 5 (p less than .001). There was also a significant rise in serum thymosin beta 4 levels on day 5 (p less than .001). Serum cortisol rose in parallel with thymosin alpha 1 on day 5 after rhinovirus inoculation, but there was no direct relationship between individual changes in cortisol and thymosin alpha 1 levels. Enumeration of peripheral blood mononuclear cell subpopulations during rhinovirus infection revealed a significant increase in total lymphocytes on day 5 (p less than .01), but not on day 3. The rise in total lymphocyte count was attributable to an increase in T lymphocytes (CD3+) (p less than .05), cytotoxic/suppressor (CD8+) cells (p less than .01) and natural killer (CD16+ cells) (p less than .05). This is the first report of thymic hormone modulation by a virus, and suggests that local rhinovirus infection of the upper respiratory tract has systemic effects and induces cellular immune responses.
