During viremia the virus preferentially infected memory T-cells, initially central memory T-cells and subsequently effector memory T-cells. In lungs, SVV infected alveolar myeloid cells and T-cells. Except for pneumonitis, pathology produced by SVV-EGFP was less compared to SVV-wt. All monkeys developed fever and skin rash. The SVV-infected cell types and virus kinetics were determined by flow cytometry and immunohistochemistry, and virus culture and SVV-specific real-time PCR, respectively. To identify the host cell types involved in virus dissemination and pathology, we infected African green monkeys intratracheally with recombinant SVV expressing enhanced green fluorescent protein (SVV-EGFP) and with wild-type SVV (SVV-wt) as a control. Clinical, pathological, virological and immunological features of simian varicella virus (SVV) infection of non-human primates parallel those of primary VZV infection in humans. The cell types that transport VZV from the respiratory tract to skin and ganglia during primary infection are unknown. Varicella-zoster virus (VZV) causes varicella, establishes a life-long latent infection of ganglia and reactivates to cause herpes zoster.
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