Effects of Immunopotentiating and Immunomodulating Agents on Experimental and Clinical Herpesvirus Infections

Gh, Werner; Zerial, Aurelio

doi:10.1007/978-1-4615-8021-8_19

Cited by 1 publication

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“…It has been shown earlier that C. parvum protects mice against infection with HSV-1 [ 14]. Not only macrophages and interferon, but also natural killer cells might be responsible for this effect [26]. C. parvum induces TNF in human mononuclear cells [18] and rTNF protects in vivo against infection with HSV-1 [24].…”

Section: Discussionmentioning

confidence: 99%

Colonization of adrenal glands and ovaries of mice by HSV-2 variants

Podlech

Weise

Falke

1990

Archives of Virology

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HSV-2 strain ER was shown to consist of variants with different pathogenic phenotype: Variant ER+ replicates to high titers in the adrenal glands and the ovaries but much less in the spleen; the testes were not colonized. ER+ migrates to the spinal ganglia and is highly neuroinvasive after i.p. inoculation. Variant ER- replicates 100-1,000 fold less in the adrenal glands and the ovaries, but proceeds to the spinal ganglia without invading the CNS. However, both variants are highly neuropathogenic after direct i.c. injection. We conclude that neuropathogenicity, neuroinvasiveness and the ability to replicate in the adrenal glands as well as ovaries are each determined by different sets of genes. Replication in mouse embryo fibroblasts--but not in Vero and adreno cortical carcinoma Y1 cells--is different for both strains. Also the adsorption capacity to cultured cells differs as shown by addition of D.S. 500. ER- is eliminated from the blood stream more quickly than ER+. Finally, C. parvum reduces the rate of replication of both variants in the adrenal and the ovaries. It is concluded that different adsorption and replications rates of variants ER+ and ER- in cell types critical for spread of HSV are responsible for the different pathobiological properties.

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Section: Discussionmentioning

confidence: 99%