Abstract
The immunological mechanisms involved in establishment of herpes simplex virus (HSV) latency were studied in normal and CD4+ T-cell depleted C57BL/6J mice following intravaginal infection. During transition from acute to latent ganglionic infection two consecutive processes were observed: first, clearance of infectious virus from the ganglia, and second, reduction of the number of infected ganglia.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
