Key result
HSV-2, but not HSV-1, induced recrudescent disease in chronically infected mice up to 18 months after inoculation, with infectious virus recovered from the heart and dorsal root ganglia.
This murine model demonstrates that HSV-2 can cause chronic, recrudescent infection in the heart and dorsal root ganglia, providing a potential model for investigating long-term human cardiopathies.
Establishes murine model for HSV-2 cardiac latency; leaves open relevance to human recrudescent cardiopathies.
The multiplication of HSV-1 and HSV-2 strains in the heart and the corresponding dorsal root ganglia (DRG) was examined in experimentally infected mice. Infectious HSV-1 was recovered from the heart between the second and fourth day after inoculation and 3 days later from the DRG. Both the heart and DRG yielded infectious HSV-2 from the fourth to the twenty-first day after inoculation. The HSV-2, but not the HSV-1, induced recrudescent disease in chronically infected mice up to 18 months after inoculation. These affected mice showed signs of disease similar to those observed during the acute phase of the primary infection. During the recrudescent disease, infectious HSV-2 was recovered both from the heart and DRG. The possibility of using this experimental model for investigating long-term human cardiopathies is discussed.
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Grodums et al. (1981) studied Herpes simplex virus infection. HSV-1 and HSV-2 inoculation vs. HSV-1 vs HSV-2 was evaluated on Recovery of infectious virus and induction of recrudescent disease. HSV-2, but not HSV-1, induced recrudescent disease in chronically infected mice up to 18 months after inoculation, with infectious virus recovered from the heart and dorsal root ganglia.
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