herpes
[Herpes simplex keratitis after ophthalmic surgery]

[Article in Japanese]

Miyajima S, Sano Y, Sotozono C, Yokoi N, Ishino Y, Kinoshita S.

Department of Ophthalmology, Kyoto Prefectural University of Medicine, 456 Kajii-cho, Kawaramachi, Kamigyo-ku, Kyoto 602-0841, Japan.

PURPOSE: We report 6 cases of herpes simplex keratitis after ophthalmic surgery, in eyes without clinical history of herpes simplex keratitis. CASES: These cases comprised 6 patients examined at our hospital between April 1992 and November 2001. Past operations were keratoplasty in 5 eyes and cataract surgery in 1 eye. Clinical findings and predisposing factors were evaluated retrospectively. The period between herpetic epithelial keratitis onset and ophthalmic surgery ranged from 1.5 to 79 months. Predisposing factors included corticosteroid therapy and operative wound. The herpetic epithelial lesions were dendritic ulcers in 2 eyes, geographic ulcer in 1 eye, and atypical epithelial lesions in 3 eyes; in all cases, herpes simplex virus (HSV)-DNA was detected by polymerase chain reaction (PCR) in tear fluid. All herpetic epithelial lesions healed with oral and topical acyclovir. CONCLUSIONS: When corticosteroids are used following ophthalmic surgery, physicians should be alert to the possibility of herpetic epithelial keratitis, even in patients with no clinical history of herpes simplex keratitis. PCR detection in tear fluid is helpful in diagnosing this disease.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14531315&dopt=Abstract herpes medicine



herpes
Immunodominance among herpes simplex virus-specific CD8 T cells expressing a tissue-specific homing receptor.

Koelle DM, Liu Z, McClurkan CL, Cevallos RC, Vieira J, Hosken NA, Meseda CA, Snow DC, Wald A, Corey L.

Department of Laboratory Medicine, University of Washington, Seattle, WA 98195, USA. viralimm u.washington.edu

The study of immunodominance within microbe-specific CD8 T cell responses has been challenging. We used a previously undescribed approach to create unbiased panels of CD8 cytotoxic T lymphocyte clones specific for herpes simplex virus type 2, a pathogen with a complex genome encoding at least 85 polypeptides. Circulating herpes simplex virus type 2-specific cells were enriched and cloned after sorting for expression of the skin homing-associated receptor, cutaneous lymphocyte-associated antigen, bypassing restimulation with antigen. The specificity of the resultant cytotoxic clones was determined. Clonal frequencies were compared with each other and with the total number of cytotoxic clones. For each subject within the homing receptor-positive compartment, the CD8 cytotoxic response was dominated by T cells specific for only a few peptides. Previously undescribed antigens and epitopes in viral tegument, capsid, or scaffold proteins were immunodominant in some subjects. Clone enumeration analyses were confirmed in some subjects with dominance studies by using herpes simplex mutants, vaccinia recombinants, and/or enzyme-linked immune spots. We conclude that among circulating cells expressing a homing-associated receptor, during chronic herpes type 2 infection, the CD8 T cell response becomes quite focused despite the presence of many potential antigenic peptides.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14566059&dopt=Abstract herpes medicine



herpes
Clinical and genetic risk factors of herpes zoster in patients with systemic lupus erythematosus.

Kang TY, Lee HS, Kim TH, Jun JB, Yoo DH.

Hospital for Rheumatic Diseases, Hanyang University Hospital, 17 Haengdang-dong, Seong Dong-ku, Seoul 133-792, Republic of Korea, dhyoo hanyang.ac.kr.

OBJECTIVE: The aim of this study was to determine the clinical and genetic risk factors that influence herpes zoster occurrence in patients with systemic lupus erythematosus (SLE). METHODS: Three hundred three SLE patients meeting the American College of Rheumatology criteria were enrolled in this study. Herpes zoster was diagnosed when classic grouped vesicles were noted. Medical records were reviewed retrospectively to collect clinical information. For Fc gamma receptor IIa (FcgammaRIIa) and FcgammaRIIIa genotyping, polymerase chain reaction (PCR) using allele-specific primers was performed. The PCR sequence-specific oligonucleotide probe method was utilized in human HLA-DRB1 genotyping. RESULTS: Forty-two cases (13.9%) of zoster occurred among 303 SLE patients. The incidence of zoster in patients with SLE was 32.5/1,000 patients per year. Patients who developed zoster had higher rates of lupus nephritis (P=0.018) and positive anti-Sm antibody (P=0.019). However, FcgammaRIIa and FcgammaRIIIa polymorphism and the HLA-DRB1 genotype did not influence herpes zoster occurrence. CONCLUSION: Systemic lupus erythematosus patients with lupus nephritis or anti-Sm antibody are at higher risk of herpes zoster. FcgammaRIIa (H/R131), FcgammaRIIIa (F/V176), and HLA-DRB1 genetic polymorphisms did not influence the occurrence of herpes zoster in these patients.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14593495&dopt=Abstract herpes medicine



herpes
Preliminary comparison of three LightCycler PCR assays for the detection of herpes simplex virus in swab specimens.

Whiley DM, Syrmis MW, Mackay IM, Sloots TP.

Clinical Virology Research Unit, Sir Albert Sakzewski Virus Research Centre, Royal Children's Hospital and Health Service District, Herston Road, 4029 Herston, Queensland, Australia.

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.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14605937&dopt=Abstract herpes medicine



herpes
Attenuating effect of mexiletine hydrochloride on herpetic pain in mice infected with herpes simplex virus.

Asano K, Sameshima T, Shirasawa H, Hisamitsu T.

Department of Physiology, School of Medicine, Showa University, Hatanodai, Tokyo, Japan. asanok med.showa-u.ac.jp

The influence of mexiletine hydrochloride on herpes-related pain responses was examined using mice infected with herpes virus. BALB/c mice were inoculated with herpes simplex virus (HSV; 1 x 10(6) plaque-forming units) on the right hind paw, and the contralateral hind paw was without inoculation. The changes in nociceptive threshold were examined using electric von fray meter. BALB/c mice inoculated with HSV showed a decrease in nociceptive threshold. Intraperitoneal administration of mexiletine prevented the decrease in nociceptive threshold dose-dependently in HSV-inoculated mice, which was firstly observed at a dose of 15.0 mg kg(-1), and peaked at doses more than 17.5 mg kg(-1). This antinociceptive effect of mexiletine attained peaks at 60-90 min after administration and declined gradually to non-treated levels by 150 min. Intraperitoneal administration of mexiletine at a dose of 17.5 mg kg(-1) (but not 10.0 mg kg(-1)) caused significant increase in beta-endorphin levels in the mid brain and hypothalamus of HSV-inoculated mice. However, mexiletine scarcely affected noradrenaline (norepinephrine) levels in the pons and medulla oblongata, even when HSV-inoculated mice were treated with 17.5 mg kg(-1) mexiletine. These results strongly suggested that mexiletine exerts antinociceptive effects on herpes-related pain through enhancement of beta-endorphin levels in the central nervous system in HSV-inoculated mice. It is also suggested that mexiletine will be a good candidate for an antinociceptive drug in the treatment of acute herpetic pain in man.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14607018&dopt=Abstract herpes medicine



herpes
Blocking immune evasion as a novel approach for prevention and treatment of herpes simplex virus infection.

Judson KA, Lubinski JM, Jiang M, Chang Y, Eisenberg RJ, Cohen GH, Friedman HM.

Infectious Disease Division, Department of Medicine, School of Medicine., University of Pennsylvania, Philadelphia, Pennsylvania 19104-6073, USA.

Many microorganisms encode immune evasion molecules to escape host defenses. Herpes simplex virus type 1 glycoprotein gC is an immunoevasin that inhibits complement activation by binding complement C3b. gC is expressed on the virus envelope and infected cell surface, which makes gC potentially accessible to blocking antibodies. Mice passively immunized with gC monoclonal antibodies prior to infection were protected against herpes simplex virus challenge only if the gC antibodies blocked C3b binding. Mice treated 1 or 2 days postinfection with gC monoclonal antibodies that block C3b binding had less severe disease than control mice treated with nonimmune immunoglobulin G (IgG). Mice immunized with gC protein produced antibodies that blocked C3b binding to gC. Immunized mice were significantly protected against challenge by wild-type virus, but not against a gC mutant virus lacking the C3b binding domain, suggesting that protection was mediated by antibodies that target the gC immune evasion domain. IgG and complement from subjects immunized with an experimental herpes simplex virus glycoprotein gD vaccine neutralized far more mutant virus defective in immune evasion than wild-type virus, supporting the importance of immune evasion molecules in reducing vaccine potency. These results suggest that it is possible to block immune evasion domains on herpes simplex virus and that this approach has therapeutic potential and may enhance vaccine efficacy.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14610186&dopt=Abstract herpes medicine



herpes
[Herpes simplex and varicella zoster virus infections]

[Article in German]

Lautenschlager S.

Dermatologisches Ambulatorium des Stadtspitals Triemli Zurich. stephan.lautenschlager triemli.stzh.ch

Herpes simplex virus (HSV) and varicella-zoster virus (VZV) are both human alpha-herpes viruses. They are capable of establishing latent infections in neural tissues and to reactive from these sites, determining the clinical features of the disease (primary infection versus recurrences). Infections with these viruses are common; an increased number of elderly and immunocompromised individuals will likely lead to an even higher prevalence. HSV infection--in its typical form characterized by grouped vesicles--is frequently inapparent or atypical in both primary and recurrent disease. The clinical spectrum is wide, ranging from trivial labial blisters to the most severe fatal sporadic encephalitis and neonatal infection. Seroprevalence studies in the Western world demonstrate a much higher percentage of people infected with HSV-2 than are currently identified by clinical studies. Since undiagnosed genital herpes infections are the major factor in fueling the genital herpes epidemic, awareness and more accurate diagnosis followed by therapy and counseling are mandatory. Primary VZV infection and herpes zoster are usually diagnosed clinically, but can be confirmed by virus detection methods from swabs of lesions or antibody tests. Antiviral therapy should be considered in varicella if the disease is complicated. In herpes zoster antiviral therapy should be given within 72 hours in immunocompromised patients and those at risk of postherpetic neuralgia. The availability of effective antiviral therapy makes early diagnosis most important.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14610899&dopt=Abstract herpes medicine



herpes
Latent herpes virus infection in human trigeminal ganglia causes chronic immune response.

Theil D, Derfuss T, Paripovic I, Herberger S, Meinl E, Schueler O, Strupp M, Arbusow V, Brandt T.

Department of Neurology, Klinikum Grosshadern, Ludwig-Maximilians University, Munich, Germany. dtheil brain.nefo.med.uni-muenchen.de

The majority of trigeminal ganglia (TGs) are latently infected with alpha-herpes viruses [herpes simplex virus type-1 (HSV-1) and varicella-zoster virus (VZV)]. Whereas HSV-1 periodically reactivates in the TGs, VZV reactivates very rarely. The goal of this study was to determine whether herpes virus latency is linked to a local immune cell infiltration in human TGs. T cells positive for the CD3 and CD8 markers, and CD68-positive macrophages were found in 30 of 42 examined TGs from 21 healthy individuals. The presence of immune cells correlated constantly with the occurrence of the HSV-1 latency-associated transcript (LAT) and only irregularly with the presence of latent VZV protein. In contrast, uninfected TGs showed no immune cell infiltration. Quantitative RT-PCR revealed that CD8, interferon-gamma, tumor necrosis factor-alpha, IP-10, and RANTES transcripts were significantly induced in TGs latently infected with HSV-1 but not in uninfected TGs. The persisting lymphocytic cell infiltration and the elevated CD8 and cytokine/chemokine expression in the TGs demonstrate for the first time that latent herpesviral infection in humans is accompanied by a chronic inflammatory process at an immunoprivileged site but without any neuronal destruction. The chronic immune response seems to maintain viral latency and influence viral reactivation.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14633592&dopt=Abstract herpes medicine