The latent herpes simplex virus.

Docherty, John J.; Chopan, M

doi:10.1128/mmbr.38.4.337-355.1974

Cited by 17 publications

(5 citation statements)

References 132 publications

(166 reference statements)

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“…In contrast, in patients with recurrent herpes labialis the specific IgG and IgA antibodies were not found to fluctuate significantly during the course of infection (Fig.1). These results are in agreement with previous studies that have shown that serum HSV neutralizing antibodies may fluctuate after primary infection but remain usually high and constant after recurrent infection [Docherty and Chopan, 1974;Shore and Nahmias, 1982;Klein, 1982;Sarov, 19841. A significant rise of HSV IgG antibodies was seen, however, in some cases of HSV encephalitis and in severe cases of recurrent mucocutaneous lesions [Kalimo et al, 19771. A higher GMT for HSV IgG and HSV IgA antibodies to membrane antigen was found in individuals with a previous history of recurrent HSV labialis than in seropositive individuals without a previous history of recurrent HSV infection (3 1.99 and 7.87 versus 21.44 and 5.76, respectively) (Fig.…”

Section: Discussionsupporting

confidence: 93%

Specific IgG and IgA antibodies to herpes simplex virus (HSV)‐lnduced surface antigen in patients with HSV infections and in healthy adults

Hadar

Sarov

1984

Journal of Medical Virology

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Herpes simplex virus (HSV)-specific IgG and IgA antibody response in patients with HSV infection and in healthy adults was studied by the immunoperoxidase antibody-membrane antigen (IPAMA) technique. In all HSV infections in which specific IgM antibodies were detected by enzyme-linked immunosorbent assay (ELISA), a significant rise in the titer of HSV IgG and IgA antibodies was found. In contrast, in patients with recurrent herpes labialis in which no specific HSV IgM antibodies were detected by ELISA, HSV IgG and IgA antibodies were not found to fluctuate significantly during the course of infection. A higher geometric mean titer (GMT) for HSV IgG and for IgA antibodies was found in seropositive individuals with a previous history of recurrent HSV than in seropositive individuals without a previous history of recurrent HSV infection. Nineteen of 26 HSV IgG seropositive healthy medical students without a previous history of recurrent HSV infection had HSV IgA antibodies to membrane antigen. The significance of this finding in understanding the mechanism of latency in healthy seropositive individuals without previous history of HSV recurrent infections is discussed.

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Section: Discussionsupporting

confidence: 93%

Specific IgG and IgA antibodies to herpes simplex virus (HSV)‐lnduced surface antigen in patients with HSV infections and in healthy adults

Hadar

Sarov

1984

Journal of Medical Virology

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“…but these were unsuccessful. Ho-wever, drug treatment A impairr virus, reactivation if the cultures were subsequently reduced t-o 37C (da-ta not shown).-An argument can be made for the possibility that HSV-2 is not latent, but that there is a dynamic equilibrium in the slow appearance of a small number of virus-producing cells (which ultimately die) and their replacement via cell division of neighboring uninfected cells (7,21). For the following reasons this possibility seems unlikely.…”

Section: Downloaded Frommentioning

confidence: 99%

Prolongation of herpes simplex virus latency in cultured human cells by temperature elevation

O’Neill¹

1977

J Virol

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Treatment of herpes simplex virus type 2 (HSV-2)-infected human fibroblast cells with cytosine arabinoside (ara-C) at 25 ,4g/ml resulted in complete inhibition of virus replication. Removal of ara-C after 7 days of treatment ultimately resulted in renewed virus replication, but after a delay of at least 5 days. If, however, the temperature was elevated from 370C to 39.5 to 40'C at the time of ara-C reversal, infectious HSV-2 did not reappear. As long as the cultures were maintained at 39.5 to 40'C (up to at least 128 days), HSV-2 was latent and infectious virus was undetectable. Ifthe temperature was reduced to 370C at any time during the latent period, infectious virus was always reactivated, but only after a period of incubation at 370C of at least 11 days. Infectious-center assays performed with latent cultures indicated that only a very small fraction of cells could reactivate virus. The infectious-center titer did not show significant changes during much of the period of latency. This seemed to argue against the possibility that the latent cultures were synthesizing very small amounts of infectious virus. Additional studies were aimed at determining the minimum incubation period at 370C required to reactivate infectious HSV-2. Latent cultures reduced from 39.5 to 40'C to 370C for less than 96 h did not yield infectious HSV-2, but those incubated at 370C for 96 h or more did.

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“…Indeed, these viruses bring about disease states of mucous membranes, eyes, skin, nervous system, and genitalia (14). Infections by HSV-1 or HSV-2 may be primary or recurrent; that is, after the initial infection both virus types have the ability to remain latent within the host and, when conditions are favorable, to cause recurring lesions (6). This cycle may be repeated indefinitely at regular or irregular intervals and serves as an excellent source of infection for the unwitting contact.…”

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confidence: 99%

Detection of herpes simplex virus infection of female genitalia by the peroxidase-antiperoxidase method alone or in conjunction with the Papanicolaou stain

Pearson¹,

Fleagle²,

Docherty³

1979

J Clin Microbiol

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The sensitive peroxidase-antiperoxidase (PXAPX) method individually and in conjunction with the Papanicolaou (PAP) stain was used to detect herpes simplex virus (HSV) in specimens from human female genitalia. Initial studies using a model system of HSV-1or HSV-2-infected Vero cells established (i) acetone as the most effective fixative, (ii) optimal dilutions of preimmunization and anti-HSV serum for differentiation of infected from noninfected cells, (iii) optimal concentration of 3,3'-diaminobenzidine tetrahydrochloride and H202 for maximal staining of infected cells with minimal background reaction, and (iv) removal of endogenous peroxidase with absolute MeOH. These various parameters, once established, were utilized in the PXAPX or PXAPX-PAP on human specimens from the vulva or cervix. In these specimens, examined by standard light microscopy, PXAPX-positive cells were dark brown with a single nucleus or multiple nuclei. By coupling the PAP to the PXAPX, detailed nuclear observations of PXAPX-positive cells were possible and revealed nuclear changes consistent with HSV infection, including syncytium formation, chromatin condensation, and an occasional Cowdry type A inclusion. The PXAPX and PXAPX-PAP correlated (r = 0.742) over a period of 72 h with HSV isolation from these samples. MATERIALS AND METHODS Virus. Virus stocks of HSV-1 (strain 69-85) and HSV-2 (strain 316-D) were obtained from F.

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The latent herpes simplex virus.

Cited by 17 publications

References 132 publications

Specific IgG and IgA antibodies to herpes simplex virus (HSV)‐lnduced surface antigen in patients with HSV infections and in healthy adults

Specific IgG and IgA antibodies to herpes simplex virus (HSV)‐lnduced surface antigen in patients with HSV infections and in healthy adults

Prolongation of herpes simplex virus latency in cultured human cells by temperature elevation

Detection of herpes simplex virus infection of female genitalia by the peroxidase-antiperoxidase method alone or in conjunction with the Papanicolaou stain

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