Site-restricted persistent cytomegalovirus infection after selective long-term depletion of CD4+ T lymphocytes

We have established a murine model system for exploring the ability
of a CD4 subset-deficient host to cope with cytomegalovirus
infection, and reported three findings. First, an antiviral
response of the CD8 subset of T lymphocytes could be not only
initiated but also maintained for a long period of time despite a
continued absence of the CD4 subset, whereas the production of
antiviral antibody proved strictly dependent upon help provided by
the CD4 subset. Second, no function in the defense against
infection could be ascribed as yet to CD4-CD8- T lymphocytes, which
were seen to accumulate to a new subset as a result of depletion of
the CD4 subset. This newly arising subset did not substitute for
CD4+ T lymphocytes in providing help to B lymphocytes, and was also
not effective in controlling the spread of virus in host tissues.
As long as a function of these cells in the generation and
maintenance of a CD8 subset-mediated response is not disproved,
caution is indicated with concern to an autonomy of the CD8 subset.
Third, even though with delay, the CD8+ effector cells raised in
the CD4 subset- deficient host were able of clear vital tissues
from productive infection and to restrict asymptomatic, persistent
infection to acinar glandular epithelial cells in salivary gland
tissue.