ArticleJournal of virology2001
Interleukin-12- and gamma interferon-dependent innate immunity are essential and sufficient for long-term survival of passively immunized mice infected with herpes simplex virus type 1.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 38 citations in OpenAlex.
- HSV-1 reactivation results in post-herpetic neuralgia by upregulating Prmt6 and inhibiting cGAS-STING.Brain : a journal of neurology · 2024Article
- Complement Suppresses the Initial Type 1 Interferon Response to Ocular Herpes Simplex Virus Type 1 Infection in Mice.Pathogens (Basel, Switzerland) · 2024Article
- Herpesviral infection and Toll-like receptor 2.Protein & cell · 2012Review
- CD200R1 supports HSV-1 viral replication and licenses pro-inflammatory signaling functions of TLR2.PloS one · 2012Article
- Immunobiology of herpes simplex virus and cytomegalovirus infections of the fetus and newborn.Current immunology reviews · 2010Article
- Article
- Human metapneumovirus establishes persistent infection in the lungs of mice and is reactivated by glucocorticoid treatment.Journal of virology · 2009Article
- Macrophages and cytokines in the early defence against herpes simplex virus.Virology journal · 2005Review
- The role of IL-12, IL-23 and IFN-gamma in immunity to viruses.Cytokine & growth factor reviews · 2004Review
- Murine gammaherpesvirus-68 elicits robust levels of interleukin-12 p40, but not interleukin-12 p70 production, by murine microglia and astrocytes.Journal of neurovirology · 2004Article
- Interplay between alpha/beta and gamma interferons with B, T, and natural killer cells in the defense against herpes simplex virus type 1.Journal of virology · 2004Article
- Borna disease virus multiplication in mouse organotypic slice cultures is site-specifically inhibited by gamma interferon but not by interleukin-12.Journal of virology · 2004Article
- Functional expression of chemokine receptor CCR5 on CD4(+) T cells during virus-induced central nervous system disease.Journal of virology · 2003Article
- Borna disease virus accelerates inflammation and disease associated with transgenic expression of interleukin-12 in the central nervous system.Journal of virology · 2002Article
- Use of immunostimulatory sequence-containing oligonucleotides as topical therapy for genital herpes simplex virus type 2 infection.Journal of virology · 2002Article
- Article
- Herpes simplex virus vectors elicit durable immune responses in the presence of preexisting host immunity.Journal of virology · 2002Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interferon (IFN) type I (alpha/beta IFN [IFN-alpha/beta]) is very important in directly controlling herpes simplex virus type I (HSV-1) replication as well as in guiding and upregulating specific immunity against this virus. By contrast, the roles of IFN type II (IFN-gamma) and antibodies in the defense against HSV-1 are not clear. Mice without a functional IFN system and no mature B and T cells (AGR mice) did not survive HSV-1 infection in the presence or absence of neutralizing antibodies to the virus. Mice without a functional IFN type I system and with no mature B and T cells (AR129 mice) were unable to control infection with as little as 10 PFU of HSV-1 strain F. By contrast, in the presence of passively administered neutralizing murine antibodies to HSV-1, some AR129 mice survived infection with up to 10(4) PFU of HSV-1. This acute immune response was dependent on the presence of interleukin-12 (IL-12) p75. Interestingly, some virus-infected mice stayed healthy for several months, at which time antibody to HSV-1 was no longer detectable. Treatment of these virus-exposed mice with dexamethasone led to death in approximately 40% of the mice. HSV-1 was found in brains of mice that did not survive dexamethasone treatment, whereas HSV-1 was absent in those that survived the treatment. We conclude that in the presence of passively administered HSV-1-specific antibodies, the IL-12-induced IFN-gamma-dependent innate immune response is able to control low doses of virus infection. Surprisingly, in a significant proportion of these mice, HSV-1 appears to persist in the absence of antibodies and specific immunity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.