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

Podlech, Jürgen; Weise, K.; Falke, D.

doi:10.1007/bf01311286

Cited by 13 publications

(16 citation statements)

References 21 publications

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“…The cells of the adrenal glands are known to synthesize corticosteroids and sex steroids. Estrogens might enhance susceptibility to infection, whereas testosterone results in the suppression of HSV-1 (29). It might be assumed that, following hematogenous infection, replication in the adrenal glands and ovaries of mice is directed by hormone-dependent mechanisms.…”

Section: Discussionmentioning

confidence: 99%

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Herpes Simplex Virus Type 1 Infection via the Bloodstream with Apolipoprotein E Dependence in the Gonads Is Influenced by Gender

Ramı́rez

Sastre

Alfaro

et al. 2005

J Virol

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Herpes simplex virus type 1 (HSV-1) causes disease in humans and animals. Infection usually occurs via the neural route and possibly occurs via the hematogenous route. The latter, however, is the main route by which immunosuppressed individuals and neonates are infected. Gender-dependent differences in the incidence and severity of some viral infections have been reported. To detect differences between the sexes with respect to HSV-1 colonization and disease, the characteristics of both acute and latent infections in hematogenously infected male and female mice were compared. In acute infection, the female mice had a poorer outcome: HSV-1 colonization was more effective, especially in the gonads and brain. In the encephalon, the midbrain had the highest viral load. In latent infection, brain viral loads were not significantly different with respect to sex. Significant differences were seen, however, in the blood and trigeminal ganglia: HSV-1 seroprevalence was observed in females, with no virus detected in males. In brain dissections, only the cerebral cortex of the females had viral loads statistically higher than those observed in the males. The spread of the virus to several organs of interest during acute infection was examined immunohistochemically. Female mice showed greater viral immunostaining, especially in the adrenal cortex, gonads, and midbrain. In male mice, HSV-1 was detected predominantly in the adrenal cortex. It was also found that apolipoprotein E promotes virus colonization of the ovaries, the APOE gene dose being directly related to viral invasiveness.

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Section: Discussionmentioning

confidence: 99%

“…After i.p. infection of mice, HSV-1 spreads by means of viremia to many of the visceral organs, the ovaries and the adrenal glands becoming the major replication sites (29). High levels of HSV-1 have been detected in the adrenal glands after inoculation by different routes and with different viral strains (5,17,26,30).…”

mentioning

confidence: 99%

Herpes Simplex Virus Type 1 Infection via the Bloodstream with Apolipoprotein E Dependence in the Gonads Is Influenced by Gender

Ramı́rez

Sastre

Alfaro

et al. 2005

J Virol

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“…It should be mentioned that after i.p. infection the strains IES, Len, KOS, ER +, M1CI and the wt strains colonize adrenal glands, liver and spleen; in contrast, strain E R -does not [12].…”

Section: Involvement Of Uterus Ovaries Liver and Spleen After Vaginmentioning

confidence: 91%

“…Moreover, ER + replicates strongly in the adrenals, ovaries, liver and spleen; in contrast, Pathogenesis of HSV vaginitis 37 E R -invades and replicates in these organs only very limited [12]. Both strains, however, colonize the spinal ganglia [12]. Strain Len [3,8] served as a reference strain for HSV-1.…”

Section: Cells and Virusesmentioning

confidence: 99%

Pathogenesis of HSV-1/2 induced vaginitis/vulvitis of the mouse: dependence of lesions on genetic properties of the virus and analysis of pathohistology

Podlech

Weise

Müntefering

et al. 1993

Archives of Virology

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A scoring system for herpes simplex virus (HSV) induced vaginitis/vulvitis in Balb/c mice was delineated from vaginal infections. Four degrees of vaginitis/vulvitis could be distinguished after infection with suitable strains of HSV despite nearly identical replication rates. The time course of replication, inflammation and pathohistology was compared further. Grade 0 was defined by lack of symptoms despite presence of strong replication, which was detectable at days 3-6. Focal necrotic lesions of the epithelial layer were present containing HSV-specific antigens. DNA could be detected by hybridization only in the outer zone of these areas. At day 6 these zones began to be re-epithelialized. In the vaginal lumen abundant detached epithelial cells and granulocytes were already present by day 2. Grade 1 was macroscopically characterized by a slight inflammation commencing on days 5-6. Replication and antigens in the epithelium were found on days 2-6. HSV-antigens were only detected above the basal membrane, and some infiltration with granulocytes and lymphocytes was observed below the basal membrane at day 4. Grade 2 showed strong redness and inflammation as well as hyperemia. Cellular infiltrates were present in the large antigen containing epithelial lesions and below the basal membrane. From day 4 on, neurons were HSV-antigen and DNA positive and macrophages in the stroma contained antigen. The vulva was also shown to be involved. Grade 3 exhibited prolonged severe hyperemia, and destruction of the epithelium and the stroma with necrosis and infiltration, especially of the vulva. This grading system was shown to depend on certain unknown genetic properties of HSV-strains. Neither thymidine-kinase activity, replication in macrophages, fusion activity of strains nor presence or absence of the Hpa I P-fragment were shown to be of importance for severity of vaginitis/vulvitis. Vaginitis/vulvitis was shown to be an all or none response to HSV independent of the rate of replication. The set of virus genes responsible for neuroinvasiveness after vaginal or i.p. inoculation was found to be different. The time course of replication (mainly days 3-6) and inflammation (days 5-10) indicates that inflammation seems to be a secondary immunological phenomenon induced later by the replication phase of HSV. Our system could be useful for separately testing drugs with antiviral and anti-inflammatory properties.

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“…HSV type 1 strains Wal [32] and 17 syn + [2] and type 2 strains D 316 [10], ER [28], and HG52 [37] have been described. The characteristics of the intertypic recombinants BX1 (28-1-19), FX9(5-8), RH6, R-12-3 and R-t2-5 derived from the parental strains 17 syn + (HSV-1) and HG52 (HSV-2) have been described elsewhere [23,29,5].…”

Section: Cells and Virusesmentioning

confidence: 99%

Factors influencing the interaction of herpes simplex virus glycoprotein C with the third component of complement

Huemer

Larcher

Dierich

et al. 1992

Archives of Virology

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The factors influencing the interaction of herpes simplex virus (HSV) glycoprotein C (gC) with the third component of complement (C3) were investigated in this study. The ability of gC of HSV type 1 (gC-1) to bind to the C3b fragment of C3 was found to be influenced by cell specific processing of gC-1 in a different manner, binding being remarkably enhanced in some cell lines following removal of sialic acid residues. Testing several intertypic recombinants of HSV we found that only strains expressing gC-1 exhibited binding to C3b, even though their genome consisted mainly of HSV-2 sequences in some recombinants. Expression of type-2 glycoproteins gB, gD, gE, gG, gH, and gI did not alter the ability of gC-1 to bind to C3b. Rosetting of HSV-1 infected Vero cells with C3b-coated red blood cells (EAC) was found to be temperature dependent and could be inhibited with purified C3b and anti-C3 antibodies. Polyanions like heparin or dextran sulfate were also inhibitory in a dose dependent manner, whereas C3d, neomycin and other aminoglycoside antibiotics failed to block. As the tested polyanions are also known to inhibit the infectivity of HSV, it could be speculated, that the complement binding function and the heparin-binding/attachment function of gC might be related.

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

Cited by 13 publications

References 21 publications

Herpes Simplex Virus Type 1 Infection via the Bloodstream with Apolipoprotein E Dependence in the Gonads Is Influenced by Gender

Herpes Simplex Virus Type 1 Infection via the Bloodstream with Apolipoprotein E Dependence in the Gonads Is Influenced by Gender

Pathogenesis of HSV-1/2 induced vaginitis/vulvitis of the mouse: dependence of lesions on genetic properties of the virus and analysis of pathohistology

Factors influencing the interaction of herpes simplex virus glycoprotein C with the third component of complement

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