We conclude that the increased viral titers observed in
mice experiencing psychological stress are the consequence of a
glucocorticoid-mediated reduction in the numbers of lymphocytes
responsible for resolving the initial infection.

Psychological stress and its associated increases in corticosterone are
generally immunosuppressive and contribute to increased herpes simplex
virus (HSV)-associated pathogenicity. However, the impact of stress on
local control of the initial mucosal-based HSV infection has not been
elucidated, nor have the ramifications of such failures of the immune
response in terms of viral spread. To address these gaps in knowledge,
the studies described herein sought to determine how psychological
stress and associated increases in corticosterone may increase
susceptibility to HSV encephalitis by allowing for increased viral
titers at the site of initial infection. We have shown that in mice
intranasally infected with HSV-1, a cell-mediated immune response
occurs in the nasopharyngeal-associated lymphoid tissue (NALT),
mediastinal lymph nodes (MLN), and superficial cervical lymph nodes
(CLN). However, psychological stress induced by restraint decreased the
number of lymphocytes in these tissues in HSV-infected mice.
Surprisingly, the effects of this restraint stress on HSV-specific CTL
function varied by immune tissue. Increased viral titers were found in
the nasal cavity of stressed mice, an observation which correlated with
an increased CD8+ cell response in the CLN. These findings led us to
extend our studies to also determine the ramifications of decreased
numbers of locally derived lymphocytes on viral titers following
infection. Using an approach in which the NALT was surgically removed
prior to infection, we confirmed that decreased numbers of NALT-derived
lymphocytes at the time of infection allows for increased viral
replication. We conclude that the increased viral titers observed in
mice experiencing psychological stress are the consequence of a
glucocorticoid-mediated reduction in the numbers of lymphocytes
responsible for resolving the initial infection.

PMID: 18657369 [PubMed - indexed for MEDLINE]

Psychoneuroendocrinology. 2008 Aug;33(7):951-63. Epub 2008 Jul 25.