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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The inflammatory response to herpes simplex virus infection of the cornea was studied in athymic nude (nu/nu) and heterozygote (nu/+) BALB/c mice. Although athymic mice were highly susceptible to HSV infection and died 13 to 17 days after corneal inoculation, they failed to develop necrotizing keratitis of the cornea. Heterozygote mice survived the initial virual infection, but many of these mice developed necrotizing keratitis and permanent corneal scarring. Light and electron microscopy showed numerous inflammatory cells (polymorphonuclear leukocytes and lymphocytes) in the corneas of heterozygote mice, but not in the athymic mice. These studies suggest that the immune system plays a dual role in herpes simplex virus infection of the cornea: protection against dissemination of the virus and immunopathogenesis of necrotizing keratitis in the cornea.
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PMID:Herpetic keratitis in athymic (nude) mice. 16 Aug 87

The accompanying inflammation seen in ocular HSV infection-the result of interactions between viruses and the immune response-can be both beneficial and potentially harmful to the host. An understanding of the interaction of virus-immune cells is just evolving from current advances in basic research. Based on our studies on HSV keratitis [11], the control of ocular HSV infection appears to involve an early inflammatory phase with macrophage reactivity and elaboration of MIF. Transient virus-specific lymphocytes with effector reactivity, as well as neutrophils with chemotactic activity, occur during the stromal keratitis. Finally, antibody-dependent complement-mediated lysis provides another phase of restriction of infection. Thus, a rationale for effective management and therapy of occular HSV disease must be based on an understanding of (1) the immunological and immunopathological mechanisms of corneal inflammatory disease initiated by the virus; (2) the immunological mechanisms in recovery from the disease; and (3) the host's humoral and cellular immune status during virus persistence (latency) and during recurrent episodes of infection. We hope that new information obtained from assessment of roles of the humoral and cellular immune responses in recovery from disease and in recurrent disease will provide new approaches to the management of ocular HSV infections.
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PMID:Immunology of herpes simplex virus in fection. 17 22

Athymic (nude) mice have played an important role in defining the function of the immune system and its role in infectious diseases. In the majority of these studies, heterozygous +/nu mice have been used as normal controls for the nu/nu mice, and it has been assumed that +/nu mice have essentially normal immune systems. We have compared the response of +/+, +/nu and nu/nu BALB/c mice following ocular infection with HSV-1 and have found that +/nu mice develop significantly more severe blepharitis, vascularization of the cornea, stromal keratitis and extraocular disease (herpetiform spread) than +/+ BALB/c mice. The extraocular disease was particularly severe in the +/nu mice, suggesting that factors regulating herpetiform spread of the virus are deficient in these mice. Susceptibility to lethal encephalitis did not differ between +/+ and +/nu mice. These results suggest that significant differences exist in the response to ocular HSV infection between +/+ and +/nu mice.
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PMID:Susceptibility of +/+, +/nu and nu/nu BALB/c mice to ocular herpes simplex virus infection. 128 12

Glycoprotein C (gC) of herpes simplex virus type 1 (HSV-1) is a receptor for the complement component C3b. We have previously isolated HSV-1 gC- strains (TN1, TN2 and TN3) from a patient with recurrent keratitis at three different times. These are very rare isolates because gC was thought to be essential for the virus in vivo. To determine whether gC modifies the interaction of complement with cell-free virus or virus-infected cells, we constructed gC+ recombinant viruses in which the intact gC gene of strain KOS was inserted into the TN1 virus genome. TN1 virus was inactivated by complement and TN1 virus-infected cells were lysed by complement; however, gC+ recombinant viruses became resistant to these effects of complement. These results suggest a role for gC in protection of both the virion envelope and the infected cell surface against damage by complement. TN1 virus was inactivated by complement from rats (Wistar, WKA, F344 and SD), guinea-pigs (Hartley) and humans, but not by complement from mice (C3H, DDD and BALB/c), which indicates that mice seem to be inappropriate as an experimental model for the study of HSV infection in which complement factors need to be considered.
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PMID:Glycoprotein C of herpes simplex virus type 1 is essential for the virus to evade antibody-independent complement-mediated virus inactivation and lysis of virus-infected cells. 184 74

Herpes simplex virus (HSV) latency in sensory ganglion neurons is well documented, but the existence of extraneuronal corneal latency is less well defined. To investigate the possibility of extraneuronal latency during ocular HSV infection, corneal specimens from 18 patients with quiescent herpes simplex keratitis (HSK) were obtained at the time of keratoplasty. Polymerase chain reaction (PCR) amplification followed by southern blot hybridization with a radiolabeled oligonucleotide probe was done to detect the presence of HSV-1 genome in these human corneal samples. Two pairs of oligonucleotides from the region of the HSV thymidine kinase (TK) gene and the latency-associated transcript (LAT) gene were used as primers in the PCR amplification. The DNA sequences from either the TK or the LAT gene were identified in 15 of 18 HSK corneas (83%). These results demonstrate that the HSV genome was retained, at least in part, in human corneas during quiescent HSV infection, giving further support to the concept of corneal extraneuronal latency.
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PMID:Detection of herpes simplex virus thymidine kinase and latency-associated transcript gene sequences in human herpetic corneas by polymerase chain reaction amplification. 185 32

Typical herpes simplex keratitis that developed in a 5-year-old boy was initially diagnosed cytologically in Papanicolaou-stained samples. Subsequently, an immunoperoxidase staining technique was used to identify the specific type of herpes simplex virus (HSV) in the destained cellular samples. The positive staining helped to establish the diagnosis of a type 1 HSV infection, permitting early treatment with acyclovir and subsequent complete recovery from the ocular herpetic infection. Emphasis is placed on the value of the immunoperoxidase technique for the rapid and specific diagnosis of cases of suspected HSV infection.
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PMID:Cytodiagnosis of herpes simplex keratitis by means of an immunoperoxidase technique. A case report. 299 71

We studied the interactions between rabbit polymorphonuclear leukocytes (PMN) and the RE strain of herpes simplex virus type 1 (HSV-1) to determine better the role of inflammatory cells in herpetic stromal keratitis. PMN were found to be nonpermissive for HSV replication and were unable to bind virus in the absence of antibody. However, PMN did bind and internalize HSV-antibody complexes in vitro as was demonstrated visually by electron microscopic studies and quantitatively by measurement of activity associated with radiolabeled HSV-antibody complexes. Virus used for immune complex formation was labeled with either 125Iodine or 35S-methionine. In some experiments, anti-HSV IgG used for immune complex formation was labeled with 125Iodine before incubation with virus. Use of all three radiolabeling approaches resulted in the same general pattern of binding, indicating a requirement for both antibody and virus for interaction with PMN. The activity associated with PMN was increased by preincubation with complement. The results suggest an active role for PMN in controlling HSV infection through their ability to bind and ingest virus-antibody complexes.
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PMID:Binding and internalization of herpes simplex virus-antibody complexes by polymorphonuclear leukocytes. 302 98

C3H/He and BALB/c mice were inoculated with herpes simplex virus (HSV) by corneal or intraperitoneal route. The mouse splenocytes were analyzed to determine the level and mode of cytotoxic T lymphocyte (CTL) induction by a cytotoxicity test, using HSV-infected L929 cells and 3T3 cells as the target cells. To enhance the activities of CTL, mouse splenocytes were restimulated by lipopolysaccharide-induced lymphoblasts (LPS-blasts) infected with HSV before assay. HSV infection by both corneal and intraperitoneal routes induced H-2 restricted T lymphocyte responses specific for HSV. This CTL response became detectable on day 6 in mice with herpetic keratitis and on day 4 with intraperitoneal infection, but 10 days after infection the CTL activities of both groups reached the same level. A high response level persisted as long as 28 days. These results suggest that the protective mechanism in herpetic keratitis is similar to the mechanism in intraperitoneal infection.
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PMID:Immunological studies of herpetic keratitis: induction of cytotoxic T lymphocytes in mouse splenocytes. 387 28

Complete gene synthesis methods have been used to construct analogs of human interferons (IFNs): these include a consensus of the known human IFN-alpha S, designated IFN-alpha Con1 and a variant of human IFN-gamma, designated IFN-gamma 4A. These interferons, in purified form, were used topically against herpes simplex virus type 1 (HSV-1) induced ocular keratitis in rabbits. Eyes pretreated with IFN-alpha Con1 had decreased signs of infection and a lower incidence of HSV-1 positive trigeminal ganglia (3 of 14 positive) compared to the placebo treated (10 of 14 positive). IFN-alpha Con1 was as effective as natural IFN-alpha subtypes on a units basis, despite the very high specific activity of this analog. IFN-gamma 4A used under similar conditions do not result in beneficial effects with treatments beginning 24 or 48 hr before or 4 hr after virus inoculation. Rabbits with confirmed latent HSV infection were treated topically with IFN-alpha Con1 (10(6) units per eye each day) either before or before and after attempts to intentionally reactivate the infection by bilateral iontophoresis of 6-hydroxydopamine plus topical epinephrine treatment of the corneas. These IFN-alpha Con1 treatment regimens along with intentional reactivation during latency did not: (1) lessen the frequency of inducible ocular shedding episodes; (2) alter the mean time of 3-5 days between attempts to reactive latent infection and the appearance of HSV in tears; or (3) significantly change the incidence of HSV-positive trigeminal ganglia (83-100% HSV positive).
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PMID:Human alpha and gamma interferon analogs in rabbits with herpetic keratitis. 392 22

The induction of luminol-dependent chemiluminescence in rabbit polymorphonuclear leukocytes (PMN) by a stromal keratitis causing strain (RE) of herpes simplex virus type 1 (HSV-1) was examined. Virus alone and virus infected rabbit corneal cells were unable to stimulate chemiluminescence. However, when the virus or virus infected cells were incubated in the presence of HSV-1 specific immune serum or purified IgG, a gradual chemiluminescent response was observed. Virus and virus infected cells incubated with normal rabbit serum or IgG produced little or no activity. No impairment of chemiluminescent response was observed in experiments in which rabbit PMN were exposed to HSV prior to the addition of opsonized zymosan or HSV-antibody complexes. Results suggest PMN exert antiviral activity in the presence of specific antibody and may be important factors in the inflammatory process resulting from ocular HSV infection.
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PMID:Dependence on antibody for induction of chemiluminescence in polymorphonuclear leukocytes by herpes simplex virus. 403 Feb 51


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