The correlates of protective immunity to disease-inducing viruses in humans remain to be elucidated. We determined the kinetics and characteristics of cytomegalovirus (CMV)-specific CD4 ؉ and CD8 ؉ T cells in the course of primary CMV infection in asymptomatic and symptomatic recipients of renal transplants. Specific CD8 ؉ cytotoxic T lymphocyte (CTL) and antibody responses developed regardless of clinical signs. CD45RA ؊ CD27 ؉ CCR7 ؊ CTLs, although classified as immature effector cells in HIV infection, were the predominant CD8 effector population in the acute phase of protective immune reactions to CMV and were functionally competent. Whereas in asymptomatic individuals the CMV-specific CD4 ؉ T-cell response preceded CMV-specific CD8 ؉ T-cell responses, in symptomatic individuals the CMV-specific effectormemory CD4 ؉ T-cell response was delayed and only detectable after antiviral therapy.The appearance of disease symptoms in these patients suggests that functional CD8 ؉ T-cell and antibody responses are insufficient to control viral replication and that formation of effector-memory CD4 ؉ T cells is necessary for recovery of infection.
The interrelationship between cytotoxin-associated gene A (CagA), vacuolating cytotoxin (VacA), and Helicobacter pylori-related diseases was investigated in 155 H. pylori-infected patients. Four (7%) of 60 subjects had mixed cagA+ and cagA- H. pylori infections. The H. pylori isolates from 98.3% of 121 patients with anti-CagA antibodies were cagA+. The occurrence of cagA+ H. pylori among 76 patients with peptic ulcer disease (PUD) was higher (93.4%) than among 79 patients with functional dyspepsia (FD; 64.6%) (odds ratio [OR] = 7.80; P < .001). VacA+ isolates were isolated from 56.6% of the PUD patients and 35.4% of the FD patients (OR = 2.37; P = .0132). For type I (cagA+VacA+) isolates, these numbers were 56.6% and 31.6%, respectively (P = .003). Only 4% of the 71 VacA+ isolates were cagA-. In addition, 37% of the patients with PUD were infected with cagA+VacA- H. pylori. Chi 2 results did not improve when VacA was entered into the model in the presence of cagA, indicating that only cagA is associated with PUD.
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