Chronic-Dose Acyclovir to Suppress Frequently Recurring Genital Herpes Simplex Virus Infection: Effect on Antibody Response to Herpes Simplex Virus Type 2 Proteins

Gold, D; Ashley, Rhoda; Solberg, G.; Abbo, H.; Corey, Lawrence

doi:10.1093/infdis/158.6.1227

Cited by 16 publications

(6 citation statements)

References 26 publications

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“…This is consistent with clinical results in patients undergoing acyclovir treatment, as reported by Lafferty et al (1984) and Mitchell et al (1986). Clinical observations concerning the immune response of HSV-infected patients showed a lower antibody titre in acyclovir-treated patients than in placebo-treated patients, resulting in suppression of antibody response or lymphoproliferative responses to HSV (Ashley & Corey, 1984;Bernstein et al, 1984;Lafferty et al, 1984;Mitchell et al, 1986;Erlich et al, 1988;Gold et al, 1988;Ragab et al, 1989;Kawana et al, 1995;Hu et al, 1997). Results of the present study would be applicable in interpreting those observations, although it is difficult to deny the possibility that antibody titre is dependent on the severity of skin lesions.…”

Section: Discussionsupporting

confidence: 86%

Acyclovir Treatment of Skin Lesions Results in Immune Deviation in Mice Infected Cutaneously with Herpes Simplex Virus

Sato

Fukuda

et al. 1999

Antivir Chem Chemother

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Clinical observations indicate that the antibody response to herpes simplex virus (HSV) in patients undergoing acyclovir treatment is reduced and, although the exact mechanism is not clear, some authors interpret it as immunosuppression. In order to clarify the mechanism, we cutaneously infected mice with HSV-1 and treated the resulting skin lesions with acyclovir. The immune response to infection and treatment in these mice was then analysed. Acyclovir treatment was given orally (20 mg/kg, three times daily), starting on day 0 (D0), 2 (D2) or 4 (D4) after infection and continuing until day 10. The serum antibody titre and the severity of skin lesions were significantly higher in the shortest treatment group (D4) than in the longer treatment groups (D0 and D2). In contrast, a skin test analysing delayed-type hypersensitivity (DTH) to HSV antigen showed that the D0 and D2 groups exhibited stronger DTH than the D4 group. Acyclovir treatment failed to cause a dissociation between DTH and antibody production in mice immunized with inactivated HSV antigen. However, acyclovir treatment in infected mice suppressed the development of skin lesions and resulted in a dissociation between DTH response and antibody production, indicating a typical immune deviation. This was supported by a change in the ratio of the isotype antibody IgG2a to IgG1. The treatment of skin lesions with acyclovir reduced the level of antibody response, as observed clinically. This indicates that the reduced antibody response in patients treated with acyclovir may be, at least in part, due to immune deviation and not immunosuppression.

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Section: Discussionsupporting

confidence: 86%

Acyclovir Treatment of Skin Lesions Results in Immune Deviation in Mice Infected Cutaneously with Herpes Simplex Virus

Sato

Fukuda

et al. 1999

Antivir Chem Chemother

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“…Alternatively, this diminished response could be due to an immunosuppressive effect of the drug. In this regard, Gold et al (4) reported that long-term administration of ACV did not affect levels of antibodies to cytomegalovirus and rubella virus, while it reduced levels of antibody to HSV-2-related proteins. Bernstein et al (2) also noted that an immunosuppressive effect of ACV seemed unlikely, since the drug level necessary to cause such an effect would be much greater than that detected in ACV-treated patients.…”

Section: Discussionmentioning

confidence: 99%

Class‐Specific Antibody Response in Acyclovir‐Treated and Adenine Arabinoside‐Treated Patients with Primary Genital Herpes Simplex Virus Infection

Kawana

Hashido

Koizumi

1995

Microbiology and Immunology

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Herpes simplex virus (HSV) class-specific antibody responses after primary genital herpes infection were evaluated with an enzyme-linked immunosorbent assay (ELISA) in 16 patients treated with acyclovir (ACV), given orally, and 17 patients treated with adenine arabinoside (Ara-A), given topically. ACV significantly suppressed the levels of IgM, IgA, and IgG. In the ACV-treated patients, IgM and IgG were not detected in 4 of the 16 and in 1 of the 16 patients, respectively. We must take into account this suppressive effect of ACV on antibody responses, especially on the IgM response, when serodiagnosis of HSV infection is made.

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“…Acyclovir is commonly used to treat infection with another member of the herpesvirus family, herpes simplex virus (HSV). The effect of acyclovir therapy on the humoral immune response to HSV proteins has been analyzed by sensitive techniques such as Western blot (immunoblot) analysis and radioimmunoprecipitation (3,6,13). Furthermore, functional analogies and structural homologies have been drawn between certain gene products of HSV and VZV.…”

Section: Discussionmentioning

confidence: 99%

“…Short-term oral acyclovir for the treatment of primary genital herpes in the immunocompetent host has been related to a decrease in the humoral response to specific polypeptides of HSV, including HSV gE (3,6). Acyclovir therapy also appears to delay the development of antibody to a number of different HSV-specific polypeptides, including those corresponding to glycoproteins D and E of HSV, and prolonged (6-to 12-month) daily suppression of genital herpes has been shown to decrease levels of antibodies to many major immunogens of HSV-2 (13). Aithough acyclovir therapy appears to influence the frequency and the magnitude of antibody response to different HSVspecific polypeptides, a similar effect was not present in the antibody response to VZV-specific polypeptides in children who received a short oral course of acyclovir.…”

Section: Discussionmentioning

confidence: 99%

Acyclovir treatment for varicella does not lower gpI and IE-62 (p170) antibody responses to varicella-zoster virus in normal children

1990

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The varicella-zoster virus (VZV) membrane glycoprotein gpI elicits a major immunoglobulin G antibody response after naturally acquired VZV infection; antibody to a nonglycosylated immediate-early protein, IE-62 (p170), represents a response to a nonmembrane VZV component. We evaluated antibody response to VZV gpI and IE-62 (p170) at 28 days and 1 year following infection in 34 children (ages 5 to 16 years) enrolled in a randomized placebo-controlled study of oral acyclovir for the treatment of varicella. All children were VZV antibody negative at enrollment, were previously healthy, and had laboratory-documented varicella. Compared with placebo recipients, acyclovir recipients had lower geometric mean titers by the fluorescent antibody to membrane antigen technique at 28 days (620 versus 836) but similar titers at 1 year (122 versus 122). All children had antibodies to gpI and IE-62 detectable by enzyme-linked immunosorbent assay at 28 days and 1 year. No difference in gpI at 28 days compared with 1 year was noted in acyclovir recipients. No difference in antibody to IE-62 (p170) was noted when acyclovir and placebo recipients were compared at either 28 days or 1 year. Antibody responses to gpI and IE were similar when children were stratified by age (5 to 6 years, 7 to 11 years, 12 to 16 years). A short course of oral acyclovir for the treatment of varicella did not affect antibody responses to gpI or IE-62 (p170) in healthy children at 28 days and 1 year following varicella.

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Chronic-Dose Acyclovir to Suppress Frequently Recurring Genital Herpes Simplex Virus Infection: Effect on Antibody Response to Herpes Simplex Virus Type 2 Proteins

Cited by 16 publications

References 26 publications

Acyclovir Treatment of Skin Lesions Results in Immune Deviation in Mice Infected Cutaneously with Herpes Simplex Virus

Acyclovir Treatment of Skin Lesions Results in Immune Deviation in Mice Infected Cutaneously with Herpes Simplex Virus

Class‐Specific Antibody Response in Acyclovir‐Treated and Adenine Arabinoside‐Treated Patients with Primary Genital Herpes Simplex Virus Infection

Acyclovir treatment for varicella does not lower gpI and IE-62 (p170) antibody responses to varicella-zoster virus in normal children

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