BACKGROUND: Congenital human cytomegalovirus (HCMV) infection can result in lifelong neurological deficits. Seronegative pregnant woman often acquire primary HCMV from clinically asymptomatic, but HCMV-shedding children. METHODS: Potential age-related differences in viral and immune parameters of primary RhCMV infection were examined in an oral rhesus CMV infection model in specific pathogen free macaques. RhCMV shedding was measured by real time PCR in plasma, saliva and urine. Immune parameters, including neutralizing and binding antibodies and RhCMV-specific T cell responses, were assessed in longitudinally collected blood samples. RESULTS: The oral RhCMV infection model in infant SPF rhesus macaques demonstrated that (i) the susceptibility to oral RhCMV infection declines with age, and (ii) infant macaques shed RhCMV more persistently and at higher titers compared to adult macaques. (iii) CONCLUSIONS: The oral infant RhCMV infection model appears to reflect viral pathogenesis in human HCMV-infected children. Larger studies are needed to define immune parameters associated with better control of RhCMV in adult compared to young animals.
BACKGROUND: Congenital human cytomegalovirus (HCMV) infection can result in lifelong neurological deficits. Seronegative pregnant woman often acquire primary HCMV from clinically asymptomatic, but HCMV-shedding children. METHODS: Potential age-related differences in viral and immune parameters of primary RhCMV infection were examined in an oral rhesus CMV infection model in specific pathogen free macaques. RhCMV shedding was measured by real time PCR in plasma, saliva and urine. Immune parameters, including neutralizing and binding antibodies and RhCMV-specific T cell responses, were assessed in longitudinally collected blood samples. RESULTS: The oral RhCMV infection model in infant SPF rhesus macaques demonstrated that (i) the susceptibility to oral RhCMV infection declines with age, and (ii) infant macaques shed RhCMV more persistently and at higher titers compared to adult macaques. (iii) CONCLUSIONS: The oral infantRhCMV infection model appears to reflect viral pathogenesis in humanHCMV-infectedchildren. Larger studies are needed to define immune parameters associated with better control of RhCMV in adult compared to young animals.
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