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Herpes simplex infection can appear in a wide variety of clinical presentations. The primary herpes infection can be recognized as grouped vesicles on an erythematous base which may ulcerate. Laboratory confirmation can be made by a rapid Tzanck smear or culture. When used appropriately, acyclovir is effective in treating herpes infection. The drug is available in topical and intravenous forms, and an oral form is being investigated. Acyclovir-resistant viruses have already appeared.
Previous studies from our laboratory indicated that human NK activity against HSV-infected fibroblasts (HSV-Fs) but not K562 targets was sensitive to treatment with anti-HLA-DR plus C. In the current study, we have selected Leu-11a+ (CD-16) cells by fluorescence activated cell sorting and found that although Leu-11a enriched populations lysed K562 targets in 14-h 51Cr-release assays, they were unable to kill HSV-Fs targets unless a Leu-11a-depleted population was added back to the effectors or unless known activators of NK cells (IFN-alpha or IL-2) were added to the assays. In contrast, Leu-11a-enriched populations were able to mediate ADCC against HSV-Fs in the presence of sera from HSV-seropositive individuals without the requirement for accessory cells. We have begun preliminary characterization of the accessory cells which allow lysis of HSV-Fs by NK cells: they are HLA-DR+ cells which enrich in the light density fractions of Metrizamide density gradients. They need be present in very small numbers for lysis to take place and are not MHC restricted in that heterologous add-backs between anti-HLA-DR plus C and anti-Leu-11b plus C-treated populations are capable of target cell lysis at levels similar to those achieved with the autologous add-backs. Further, the levels of lysis in heterologous add-back experiments reflected the lytic potential of the effector rather than the accessory cell donor. Finally, although the requirement for accessory cells for NK lysis has been demonstrated for fibroblasts infected with HSV-1, CMV, and VZV, lysis of HSV-infected Raji lymphoblastoid cells is relatively accessory-cell independent, indicating that the requirement for accessory cells for lysis by NK cells is not a property of all herpesvirus-infected targets.
Infection of cells with herpes simplex virus type 1 (HSV-1) induces high levels of deoxypyrimidine triphosphatase. The majority of the enzyme activity is found in infected cell nuclei. A similar activity is induced by HSV type 2 (HSV-2) which, in contrast to the HSV-1 enzyme, fractionates to more than 99% in the soluble cytoplasmic extract. Of a series of temperature-sensitive mutants of HSV-1 studied, only the immediate-early mutants in complementation group 1-2 (strain 17 mutants tsD and tsK and strain KOS mutant tsB2) induced reduced levels of triphosphatase at nonpermissive temperature. Of a series of temperature-sensitive mutants of HSV-2 strain HG52, ts9 and ts13 failed to induce wild-type levels of the enzyme at nonpermissive temperature; ts9 was the most defective mutant with regard to triphosphatase expression of both herpes simplex virus serotypes. After shift-up from permissive to nonpermissive temperature, triphosphatase activity in cells infected with ts9 decreased rapidly, whereas all other mutants continued to exhibit enzyme levels comparable with controls kept at the permissive temperature. The type 1-specific nuclear expression of the triphosphatase was mapped physically by the use of HSV-1 x HSV-2 intertypic recombinants, based on enzyme levels different by more than two orders of magnitude found in nuclei of HSV-1- and HSV-2-infected cells. The locus for the type-specific expression maps between 0.67 and 0.68 fractional length on the HSV genome.
Evidence is presented that the herpes simplex virus type 2 glycoprotein previously designated gF is antigenically related to herpes simplex virus type 1 gC (gC-1). An antiserum prepared against type 1 virion envelope proteins immunoprecipitated gF of type 2 (gF-2), and competition experiments revealed that the anti-gC-1 component of the antiserum was responsible for the anti-gF-2 cross-reactivity. An antiserum prepared against fully denatured purified gF-2, however, and three anti-gF-2 monoclonal antibodies failed to precipitate any type 1 antigen, indicating that the extent of cross-reactivity between gC-1 and gF-2 may be limited. Several aspects of gF-2 synthesis and processing were investigated. Use of the enzymes endo-beta-N-acetylglucosaminidase H and alpha-D-N-acetylgalactosaminyl oligosaccharidase revealed that the fully processed form of gF-2 (about 75,000 [75K] apparent molecular weight) had both complex-type N-linked and O-linked oligosaccharides, whereas newly synthesized forms (67K and 69K) had only high-mannose N-linked oligosaccharides. These last two forms were both reduced in size to 54K by treatment with endo-beta-N-acetylglucosaminidase H and therefore appear to differ only in the number of N-linked chains. Neutralization tests and radioiodination experiments revealed that gF-2 is exposed on the surfaces of virions and that the 75K form of gF-2 is exposed on cell surfaces. The similarities and differences of gF-2 and gC-1 are discussed in light of recent mapping results which suggest collinearity of their respective genes.
A solid-phase radioimmunoassay method was used for the detection of herpes simplex virus (HSV) immunoglobulin M (IgM), IgA, and IgG antibodies within the central nervous system in 11 patients with acute HSV encephalitis. Serial cerebrospinal fluid (CSF) and serum specimens were sampled during the observation periods, extending up to 43 months after onset. The clinical diagnosis of HSV encephalitis was confirmed demonstrating virus or virus antigen in the central nervous system in four patients and with significant HSV antibodies in CSF in all the patients. In acute stage CSF HSV antibodies of a significant level were demonstrated in one of four samples taken on days 3--4 after onset, and in samples taken on days 6--8 in five of nine patients. CSF HSV antibodies of a significant and high level were detected in all samples taken from day 10 after onset. Intrathecal production of HSV IgM and IgA antibodies lasted from 7 weeks to 43 months during the observation periods. All patients had persistent intrathecal production of HSV IgG antibodies as well as of oligoclonal IgG during the total observation periods up to 43 months.
Herpes-associated erythema multiforme can be controlled by continuous suppressive treatment with oral acyclovir. Erythema multiforme is not prevented if oral acyclovir is administered after a herpes simplex recurrence is evident and it is of no value after erythema multiforme has occurred. There is some question whether continuous topical treatment with acyclovir to sites of recurrent herpes will sometimes prevent erythema multiforme. Erythema multiforme may be precipitated by orolabial and genital recurrences and by recurrences on skin of the buttocks and other sites. Some herpetic recurrences are associated with erythema multiforme and some are not and episodes of erythema multiforme are not always associated with clinical herpetic recurrences.
Herpes is one of the most widespread human viral pathologies. The article depicts a special modification of polymerized chain reaction--(PCR)--(referred to as "nested"), which has a higher sensitivity, specificity and reliability as compared to the ordinary PCR, and which is designed to detect the herpes viruses. The method was initially tested at purified preparation of viral DNA, and later--at clinical materials obtained from patients and healthy donors. Secretions from the urogenital tract (smears), scrapes from the urogenital tracts and urinal cellular samples were examined in patients. Herpes simplex was detected in all cases. As for the healthy people, the identical examinations produced in them mainly the negative findings. Therefore, the nested PCR is a simple, sensitive and effective instrument in the diagnostics and prevention of herpes; it can be recommended for a comprehensive usage in medical practice.
Using rabbit antiserum hyperimmune to herpes simplex virus (HSV) type 1, the expression of HSV-common surface antigen(s) was studied by indirect immunofluorescence tests in cells transformed by HSV type 2 and in derived tumor cells. The following results were obtained. (i) Antiserum to HSV type 1 reacted specifically with surface antigen present on the plasma membrane of both HSV type 2-infected and HSV type 2-transformed hamster cells. (ii) The expression of this antigen was enhanced in the absence of active protein synthesis in transformed cells, but not in tumor cells, after culture for 3 to 5 h at 37 degrees C. (iii) This enhancement of expression was maintained for 20 h in the presence of actinomycin D, but this prolonged expression required active protein synthesis. (iv) The enhancing effect observed in the presence of actinomycin D continued for some time after removal of the drug, for example, for 20 h after 5 h of treatment with 2 microgram/ml of actinomycin D per ml. Actinomycin D had no detectable effect on antigen expression in tumor cells. (v) The protease inhibitor antipain inhibited the actinomycin D-enhanced expression without causing significant cell damage but did not modify the transient enhanced expression of antigen when cells were seeded in the absence of actinomycin D. These results indicate that in transformed cells antigen expression can be enhanced in at least two ways.
Genital herpes is a sexually transmitted disease caused by the herpes simplex virus. Following the initial infection the virus becomes latent in the sacral ganglia. Approximately 80% of patients are then subject to milder but unpredictable recurrences and may shed the virus even when they are asymptomatic. The disorder causes concern because genital herpes in the mother can result in rare but catastrophic neonatal infection and because of a possible association between genital herpes and cancer of the cervix. No effective treatment is as yet available. Weekly monitoring for virus by cervical culture from 32 weeks' gestation is recommended for women with a history of genital herpes and for those whose sexual partner has such a history.
Treatment of mice with LPS at the time of priming with herpes simplex virus type 1 (HSV1) causes the preferential activation of virus-specific T suppressor (Ts) cells. These Ts cells can transfer suppression to the efferent limb of a DTH response. Priming under these conditions is associated with enhanced cell-recruitment to the inoculation site, but had no effect on virus clearance. The induction of suppression was abrogated by pretreatment of mice with cyclophosphamide or indomethacin. LPS had no effect on the antibody response to HSV1 during acute infection, although treated mice showed a raised antibody titre one month after inoculation. Susceptible mice inoculated with HSV1 and given LPS showed protection, both from lethal herpes encephalitis and from demyelination within the CNS as reflected by ear paralysis. These results imply that, during some stages of acute infection, T cell effector mechanisms may themselves mediate tissue damage. At such times, Ts cells may perform a beneficial role leading to a reduction in pathology.
Herpes simplex infections of the perianal skin and anal canal are not uncommon, as evidenced by the present series of 16 cases, but have rarely been reported in the literature of the past. They are caused by the HSV-2 virus, which is also associated with genital lesions. There is abundant evidence that anogenital herpes is a venereal disease. Anal herpes is most commonly transmitted by anal intercourse. When the infection is present inside the anal canal, especially in a primary attack, the pain can be quite dibilitating. The diagnosis can usually be made on clinical grounds by recognizing the typical vesicles or aphthous ulcers, together with inguinal lymphadenopathy. The disease is self-limiting, but may be recurrent. Asymptomatic homosexuals may represent a large reservoir of the disease, which appears to be on the increase in our society. Cytology, immunofluorescence, viral cultures and serologic tests can be used for laboratory confirmation of the diagnosis. Newer methods of treatment with vaccine containing heat-inactivated virus, and use of photoinactivation following topical application of heterotricyclic dyes, show promise.
Herpes simplex should be recognized as a precipitating factor, a secondary invader, or an imitator of chronic benign familial pemphigus. Results of Tzanck smear and viral culture can confirm the presence of the pathogen so that acyclovir therapy can be instituted.
Herpes simplex virus infections in mice offer a useful model system for the study of viral pathogenesis. These infections usually result in complete recovery and involve a number of host defence mechanisms, including the action of macrophages, interferon production and specific immunological responses.
Herpes simplex encephalitis is a rapidly progressive disease in neonates and adults. Mortality is high, and there are severe neurologic sequelae in survivors. The reasons for centripetal transfer of virus to the brain are not fully understood. Prompt diagnosis followed by antiviral therapy with acyclovir significantly improves the prognosis. Controversy surrounds the need for brain biopsy before antiviral therapy is started.
Herpes simplex encephalitis (HSE) is commonly treated empirically with acyclovir without confirmatory brain biopsy. Three consecutive adults with molecularly verified mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome presented with, and were treated for, apparent HSE. MELAS syndrome in adults may present as an atypical, recurrent form of HSE and should be added to the list of neurologic diseases that can mimic HSE.
Herpes simplex virus isolation by conventional cell culture in primary rabbit kidney cells (RK) was compared with Cultureset (CS). At 24 h CS was more sensitive (31 versus 25 of 55 isolates detected) than RK, but at 48 h there was little difference (43 detected by CS, 46 by RK). CS stained at 48 h was significantly less sensitive (78.2%) than RK observed for 1 week. CS stained at 24 or 48 h was not an acceptable substitute for RK observed for 1 week.
Herpes simplex virus commonly causes 'cold sores', the virus often becoming latent after the primary infection and recrudescing at intervals. Six glycoproteins have been described in the virion and in the membranes of infected cells; much of the host's immune response is directed against these molecules. The functions of individual glycoproteins in the disease process and in the induction of different components of the immune response are beginning to be unravelled, which should help provide a strategy for the creation of an effective subunit vaccine against the virus.