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Herpes simplex virus may cause esophagitis, usually in patients with malignant neoplasms or immunocompromise. We have reported three cases of herpes simplex esophagitis in healthy young men, all of whom had positive mucosal biopsy culture for herpes simplex virus. All three patients recovered quickly without specific therapy.
Herpes simplex virus and varicella-zoster virus are common infections and are seen frequently in clinical practice. Infection with these viruses results in cutaneous lesions that may be diagnosed clinically, but widely available laboratory testing is useful for confirmation. Asymptomatic herpes simplex virus shedding, or "subclinical reactivation," likely occurs in all persons infected with herpes simplex virus and results in the transmission of virus despite the absence of signs or symptoms that suggest active infection. Oral and intravenous acyclovir are effective in treating initial and recurrent herpes simplex and varicella-zoster virus infections. The daily administration of oral acyclovir as suppressive therapy is effective in patients with frequently recurring genital infection with herpes simplex virus by reducing the number of symptomatic recurrences and the frequency of asymptomatic virus shedding. Two new antiviral agents, famciclovir and valacyclovir hydrochloride, have been approved for the short-term treatment of recurrent genital herpes simplex virus and recurrent zoster in nonimmunocompromised hosts. Famciclovir and valacyclovir demonstrate superior pharmacokinetics compared with acyclovir and allow for less frequent daily dosing with higher achievable serum drug concentrations. The attenuated live varicella virus vaccine is now available in the United States and prevents primary varicella-zoster virus infection in susceptible children and adults.
It is known that nucleic acids from formalin-fixed tissues are not nearly as good templates for DNA amplification as those extracted from fresh tissues. However, specimens stored in most pathologic archives are initially fixed in formalin. The possibility of an infectious etiology of several diseases including Alzheimer's underscores the usefulness of archived tissue in assessing the association of infectious agents with specific pathology. In this report, we describe in detail a method resulting in robust amplification of HSV1 and Human Herpes type (HHV) 5 viral DNA targets using formalin-fixed Alzheimer brain frontal and temporal tissue as source of amplification template. Herpes simplex type 2 viral DNA was not detected in the limited samples examined in this study. Amplicons were verified by sequence analysis. Brain tissue stored in formalin longer than 1 year prior to post-formalin-fixation analysis gave rise to significantly shorter amplicons consistent with the observation that template DNA integrity decreases significantly with increasing time of storage in formalin. Thus, this report should be useful in PCR-based investigations assessing the regional presence of viral DNAs in formalin-fixed brain tissue.
We report on the separate PCR cloning and subsequent expression and purification of the large (R1) and small (R2) subunits from equine herpes virus type 4 (EHV-4) ribonucleotide reductase. The EHV-4 R1 and R2 subunits reconstituted an active enzyme and their abilities to complement the R1 and R2 subunits from the closely related herpes simplex virus 1 (HSV-1) ribonucleotide reductase, with the use of subunit interaction and enzyme activity assays, were analysed. Both EHV-4 R1/HSV-1 R2 and HSV-1 R1/EHV-4 R2 were able to assemble heterosubunit complexes but, surprisingly, neither of these complexes was fully active in enzyme activity assays; the EHV-4 R1/HSV-1 R2 and HSV-1 R1/EHV-4 R2 enzymes had 50% and 5% of their respective wild-type activities. Site-directed mutagenesis was used to alter two non-conserved residues located within the highly conserved and functionally important C-termini of the EHV-4 and HSV-1 R1 proteins. Mutation of Pro-737 to Lys and Lys-1084 to Pro in EHV-4 and HSV-1 R1 respectively had no effects on subunit assembly. Mutation of Pro-737 to Lys in EHV-4 R1 decreased enzyme activity by 50%; replacement of Lys-1084 by Pro in HSV-1 R1 had no effect on enzyme activity. Both alterations failed to restore full enzyme activities to the heterosubunit enzymes. Therefore probably neither of these amino acids has a direct role in catalysis. However, mutation of the highly conserved Tyr-1111 to Phe in HSV-1 R1 inactivated enzyme activity without affecting subunit interaction.
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In cases of herpes simplex encephalitis, a low density lesion in the temporal lobe is a common CT finding, whereas hemorrhagic lesion is rarely observed on CT in this disorder despite the frequent occurrence on pathologic studies. Two cases of hemorrhagic lesion observed on CT in herpes simplex encephalitis are reported, and atypical CT findings of herpes simplex encephalitis is discussed.
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.
BACKGROUND: Transplacental intrauterine infection with herpes simplex virus is an extremely rare complication of primary herpes simplex in pregnancy. Overwhelming fetal sepsis might result in multiorgan failure, including fetal brain death. CASE: A 34-year-old multigravida presented with a healing ulcerative genital rash at 16 weeks' gestation. She subsequently reported at 28 weeks' gestation that there had been no fetal movements for 2 weeks. A cardiotocograph showed absent short- and long-term variability. At delivery, an infant was born with disseminated herpes simplex infection in poor condition. Active treatment was subsequently withdrawn, and postmortem examination confirmed disseminated herpes simplex type 2 infection. CONCLUSION: Transplacental herpes simplex is a rare and potentially lethal form of congenital herpes. Overwhelming in utero sepsis should be considered in the differential diagnosis of fetal brain death.
Both herpes simplex virus (HSV) type I and HSV type 2 can cause genital herpes. Because the infection is chronic, genital herpes has become the most common sexually transmitted disease among women. The prevalence of the HSV-2 antibody among women in the United States is 26%, although genital herpes has been diagnosed in only a small proportion (10-25%) of individuals with HSV-2 antibodies. Herpes simplex virus type I is becoming a more frequent cause of genital herpes, especially among young women. Overall,HSV-I seroprevalence in the United States is estimated at 67%, although sero-logic data do not provide information about site of infection. Recent advances in diagnostic methods and therapeutic options are likely to change the management of genital herpes.
A neonate with herpes simplex pneumonia is described. Herpes simplex infection should be considered in the differential diagnosis of pneumonia in newborn infants, even in the absence of clinically apparent herpes in the mother.
PURPOSE: To report three cases in which herpes simplex keratitis developed after initiation of latanoprost therapy. METHODS: Case report. RESULTS: One patient with a history of herpes simplex keratitis had recurrence of herpes simplex keratitis with latanoprost treatment, resolution when latanoprost was stopped, and another recurrence when rechallenged with latanoprost. A second patient with a history of herpes simplex keratitis had bilateral recurrence with initiation of latanoprost; antiviral therapy could not eradicate herpes simplex keratitis until the latanoprost was discontinued. The third patient with latanoprost-associated herpes simplex keratitis cleared with the discontinuation of latanoprost and start of antiviral therapy; reinstitution of latanoprost with prophylactic antiviral medication kept the cornea clear, but as soon as the antiviral suppression was discontinued, herpes simplex keratitis reappeared. CONCLUSION: Latanoprost, among its diverse pharmacologic effects, may mediate inflammation in the eye. Prostaglandins may be a final common pathway for stimulating recurrence of herpes simplex keratitis. Clinicians should be aware of this possible association.
There are six herpes viruses, three of which, the varicella-zoster virus and the herpes simplex viruses types 1 and 2, are of particular concern to patients and staff in critical care units. These viruses, especially in their reactivated states, may present atypically in critically ill and immune-suppressed patients, and, by the time the diagnosis is made, exposures of other patients and clinicians may have occurred. Pregnancy and immunosuppressed states can result in severe, even life-threatening varicella-zoster virus infections in susceptible adults. Similarly, nosocomial herpes simplex virus infections can have serious consequences for exposed patients and staff. An additional problem after herpes simplex virus infection is the potential of lifelong and possibly frequent recurrences. In this article, the manifestations, modes of transmission, and treatment will be discussed. Special emphasis will be placed on describing the types of patients who are at high risk of presenting with varicella-zoster virus or herpes simplex virus infection so that physicians and nurses can use appropriate preventive measures to avert nosocomial infections in patients and staff.
Three Herpes Simplex Virus LightCycler polymerase chain reaction assays were compared for the detection of herpes simplex virus in 48 swab specimens. The assays comprised of one in-house assay and two commercial kits: the Artus HSV LC RealArt PCR kit and the Roche LightCycler HSV 1/2 Detection kit. On the whole, the three assays had comparable sensitivities. However, differentiation of herpes simplex virus types 1 and 2 by melting curve analysis was problematic in all assays. Overall, the results highlight the limitations of typing herpes simplex virus by melting curve analysis.
Of nine herpes simplex virus 1 strains (from lip, mouth, throat, cornea, or brain) only five produced enough nonvirion antigen (i.e., not a structural component of the virus) to be detected by complement fixation with specially prepared, virion-absorbed, type-1 guinea pig antisera, while the remaining four strains produced only enough of the same antigen to induce specific antibody in hyperimmunized guinea pigs. While the type 1 virion antiserum used reacted equally well by complement fixation with the type 1 and type 2 strains, the type 1 nonvirion antisera failed to react with nonvirion antigens produced by three type-2 (genital) strains. However, type 2 nonvirion antiserum reacted equally well with the three type 2 and four type 1 nonvirion antigens that were tested. It appears, therefore, that while herpes simplex virus 1 codes only for type 1 nonvirion antigen, herpes simplex 2 codes not only for an immunologically distinct type 2 nonvirion antigen but also for enough type 1 nonvirion antigen to stimulate antibody production for it. Herpes simplex 2 nonvirion antigen exhibited the same properties as type 1, i.e., its activity was lost on storage at 4 degrees for 15 days, it was sedimented by centrifugation at 33,360 x g for 1 hr, and the maximum concentration was found at 3 hr in guinea pig kidney culture cells, but at 24 hr in HEp 2 and rabbit kidney culture cells. Sera from patients with genital lesions caused by herpes simplex virus 2, as well as from randomly selected adults, failed to react with either type 2 or type 1 nonvirion antigens. Accordingly, the basic information is now available to permit the use of these nonvirion antigens to determine the possible role of the herpes simplex viruses in certain human cancers.
Herpes simplex virus type 2 is considered by many venereologists as the predominant serotype among those patients suffering from genital herpes. However, identification of genital isolates obtained from 16 through 20, and 31 through 40 year old individuals among our female patient population shows a predominance of HSV-1 infections. These data suggest that the "above the waist"-"below the waist" epidemiologic patterns commonly ascribed to reflect a prevalence of HSV-1 and HSV-2 infections respectively, may no longer be appropriate in certain patient populations.