Case Of Varicella Zoster Virus Research Articles

Immunological Responses to Varicella-Zoster Virus (VZV) in Basrah with Special Emphasis on the Pattern of Exposure

The study aimed on the study of pattern of exposure and immunological responses to varicella-zoster virus (VZV) infection. Methods: A seroepidemiological study was carried out on 92 blood samples collected from children in primary health care centers and outpatient clinics of Al-Sader Teaching and Basrah maternity and children hospital during the period from January 2007 till March 2008. Serological responses were investigated by an enzyme-linked immunosorbent assay (ELISA) to detect VZV IgG antibody and cellular responses was detected by Erythrocyte rosette (E-Rosette) formation test. Results: The overall VZV- antibody prevalence was 53.3% for both serologic and cellular responses. The degree and pattern of exposure to VZV cases plays important role in the seroconversion and responses to VZV infections. The greatest responses observed in those with direct contact (household) with chickenpox cases (68.6% and 74.3%) and the direct contact acquired from VZV infected mothers (80% for both serologic and cellular responses). Exposure to typical chickenpox cases confers higher serologic and cellular responses (75% and 94.4% respectively). Cellular responses to VZV infections lasted longer than that for serologic responses. Sever VZV infections confers significantly higher levels of immunity (100%) and the complication post VZV infections (Pneumonia and encephalitis) mostly associated with sever cases at earlier age groups rather than the mild VZV cases. The differences in immune responses to VZV infections between male and females was significant (P

Varicella zoster virus vasculopathy: A treatable form of rapidly progressive multi-infarct dementia after 2 years' duration

We describe an extraordinarily protracted case of varicella zoster virus (VZV) multifocal vasculopathy in a man who presented initially with ischemic optic neuropathy and then suffered 4 episodes of stroke manifesting as multi-infarct dementia over a 2-year period. Brain magnetic resonance imaging (MRI) and angiography (MRA) revealed cortical and subcortical infarctions as well as vasculitic occlusion and stenosis. The patient was treated with corticosteroids and later with cyclophosphamide. More than 2years after the onset of neurological disease, two cerebrospinal fluid (CSF) examinations revealed the presence of anti-VZV IgG antibody with reduced serum-to-CSF ratios of anti-VZV IgG compared with ratios for total IgG and albumin, indicative of intrathecal synthesis of anti-VZV IgG. After definitive diagnosis, immunosuppressive drugs were discontinued and he was treated with intravenous acyclovir; both mental status and gait improved and no further episodes of neurological dysfunction ensued. The favorable outcome in this patient indicates that VZV vasculopathy can be treated successfully even after 26months. VZV must be considered as a possible cause of neurological disease in any patient with idiopathic multifocal vasculopathy.

Varicella Zoster Virus Vasculopathy in Adult: A Rare Case Report

Varicella-zoster virus (VZV) is the only virus in human beings that has been shown to replicate in arteries and produce vasculopathy. Varicella-zoster virus (VZV) vasculopathy is a serious entity, producing considerable neurologic deficit and sometimes death. VZV produces either large vessel or small vessel vasculopathy in the CNS. Immunocompetent patients commonly have large-vessel disease whereas immunocompromised usually develop small-vessel vasculopathy. Patients presenting with neurological deficits that are suggestive of a vasculopathy, even in the absence of rash or CSF pleocytosis, should undergo virological testing for VZV. Here we present a rare case of varicella zoster virus induced vasculopathy.

Les complications oculaires au cours de l’infection par le VIH : expérience du pôle d’excellence Nord du Maroc

HIV infection is associated with a wide variety of ophthalmic manifestations. The objective of this study was to identify the ocular complications of HIV/AIDS in Morocco.A retrospective study conducted in the internal medicine department of the Rabat Teaching Hospital between 1998 and 2008. All HIV-positive patients were retained for the study. Each patient had an exhaustive ocular examination.Of 115 ophthalmologic examinations, 28 were abnormal. Twenty-seven patients had stage C HIV infection and one patient was in stage A. The ocular manifestations were: 21 cases of ocular HIV-related anomalies (microangiopathies), four cases of cytomegalovirus (CMV) retinitis, one case of toxoplasmosis chorioretinitis, one case of CMV retinitis associated with toxoplasmosis chorioretinitis, two cases of Cryptococcus neoformans infection, two cases of varicella-zoster virus (VZV) retinitis, and one case of conjunctival Kaposi sarcoma. The CD4 count average was of 86±91/mm(3). Twenty-six patients had a CD4 count lower than 200/mm(3). Progression was favorable in 85 % of the cases, with three cases of blindness: bilateral in a case of VZV retinitis and unilateral in two cases of CMV retinitis and toxoplasmosis chorioretinitis.CMV infection is the main ocular opportunistic infection in our series. However, Highly Active Antiretroviral Treatment (HAART) may be the cause for the decline in the prevalence of ocular diseases and visual impairment in HIV/AIDS.

Varicella Zoster Virus (VZV) in Solid Organ Transplant Recipients

-herpesvirus family. VZV is presentworldwide and is highly infectious. Primary infection leadsto acute varicella or ‘chickenpox,’ usually from exposureeither through direct contact with a skin lesion or throughairborne spread from respiratory droplets (1,2). After initialinfection, VZV establishes lifelong latency in cranial nerveanddorsalrootganglia,andcanreactivateyearstodecadeslater as herpes zoster (HZ) or ‘shingles’ (3). More than90% of adults in the United States acquired the disease inchildhood, while the majority of children and young adultshave been vaccinated with the live virus vaccine (2,4).Primary varicella typically presents with fever, constitu-tional symptoms and a vesicular, pruritic, widely dissem-inated rash that primarily involves the trunk and face (5).Thesymptomsusuallyresolvewithin7–10days,butinrarecases primary varicella leads to more severe disease andvisceral invasion. Complications, such as hepatitis, pancre-atitis, pneumonitis and encephalitis are infrequent but canbelife-threatening;adultsandveryyoungchildrenaremorelikely to develop such complications from primary infection(6,7). Rates of hospitalization and mortality due to varicellahave dropped with the institution of routine childhood vari-cella vaccination (8,9).Nearly all patients with HZ develop an exanthem of vesic-ular lesions in a dermatomal distribution. The annual inci-dence of HZ in the general population is 1.5–3.0 cases per1000 persons (2), and is estimated to occur in up to 20%of individuals during their lifetime (10). Secondary compli-cations such as bacterial superinfection and postherpeticneuralgia (PHN), or chronic neuropathic pain at the site ofHZ, lead to increased morbidity (11).Over 90% of adult solid organ transplant (SOT) recipientswill be seropositive for VZV. Rates are lower in pediatrictransplants(12,13),butimmunitywillincreaseasuptakeofvaricella vaccine improves. Varicella is rare in adult SOT re-cipients,butcanbedevastating,withvisceralinvolvement,severe skin disease, and disseminated intravascular coag-ulation (14–19). HZ is a frequent infectious complication inSOT recipients with an incidence of approximately 8–11%during the first 4 years posttransplant (20–22). Invasive dis-ease and dissemination similar to that seen in primary VZVinfection are uncommon but have been reported in SOTand other immunocompromised populations, and level ofimmunosuppression may alter the risk of developing thesecomplications (17,23,24). Rates of PHN in SOT recipi-ents may also be higher than in immunocompetent popu-lations (22).

Varicella-zoster virus vasculopathy and central nervous system immune reconstitution inflammatory syndrome with human immunodeficiency virus infection treated with steroids

Immune reconstitution inflammatory syndrome (IRIS) is widely recognized and rarely involves the central nervous system (CNS). Patients with acquired immunodeficiency syndrome (AIDS) are at an increased risk for developing CNS-IRIS upon initiation of highly active antiretroviral therapy (HAART). This syndrome can be fatal and requires extreme vigilance in determining if a treatable underlying opportunistic infection exists. We report here a case of varicella-zoster virus (VZV) vasculopathy and CNS-IRIS in a human immunodeficiency virus (HIV)-infected patient who required prolonged steroid treatment for clinical stabilization. There are no established treatment regimens for IRIS and the use of corticosteroids in this syndrome remains controversial. Similar to our patient, severe cases of CNS-IRIS may benefit from high-dose intravenous corticosteroid treatment followed by an oral prednisone taper.

Two cases of varicella zoster virus meningitis found in pediatric patients after bone marrow transplantation despite valaciclovir prophylaxis and without skin lesions

Two cases of varicella zoster virus (VZV) meningitis are described in an 18-year-old girl and an 18-year-old boy. They occurred, respectively, 9 days and 9 months after allogeneic bone marrow transplantation. VZV nucleic acid was detected in the cerebrospinal fluid during the 1st week of illness. This recurrence occurred despite valaciclovir prophylaxis and without skin lesions. The two patients received aciclovir intravenously and immunoglobulins infusion. They responded to treatment and their clinical state improved rapidly.

Complex formation facilitates endocytosis of the varicella-zoster virus gE:gI Fc receptor.

Open reading frames within the unique short segment of alphaherpesvirus genomes participate in egress and cell-to-cell spread. The case of varicella-zoster virus (VZV) is of particular interest not only because the virus is highly cell associated but also because its most prominent cell surface protein, gE, bears semblance to the mammalian Fc receptor Fc gammaRII. A previous study demonstrated that when expressed alone in cells, VZV gE was endocytosed from the cell surface through a tyrosine localization motif in its cytoplasmic tail (J. K. Olson and C. Grose, J. Virol. 71:4042-4054, 1997). Since VZV gE is normally found in association with gI in the infected cell, the present study was directed at defining the trafficking of the VZV gE:gI protein complex. First, VZV gI underwent endocytosis and recycling when it was expressed alone in cells, and interestingly, VZV gI contained a methionine-leucine internalization motif in its cytoplasmic tail. Second, VZV gI was found by confocal microscopy to colocalize with VZV gE during endocytosis and recycling in cells. Third, by a quantitative internalization assay, VZV gE:gI was shown to undergo endocytosis more efficiently (steady state, 55 to 60%) than either gE alone (steady state, approximately 32%) or gI alone (steady state, approximately 45%). Further, examination of endocytosis-deficient mutant proteins demonstrated that VZV gI exerted a more pronounced effect than gE on internalization of the complex. Most importantly, therefore, these studies suggest that VZV gI behaves as an accessory component by facilitating the endocytosis of the major constituent gE and thereby modulating the trafficking of the entire cell surface gE:gI Fc receptor complex.

Successful treatment of varicella zoster virus meningoencephalitis in patients with AIDS

Neurologic complications are common in patients with AIDS. Herpes zoster is a common early manifestation of HIV infection, but there have been few reports of encephalitic complications and nearly all have been postmortem. We report four cases of varicella zoster virus (VZV) meningoencephalitis diagnosed and treated antemortem, and briefly review the relevant literature. Mount Zion Medical Center, San Francisco, California, USA. Four HIV-positive male patients with antibodies to VZV in their cerebrospinal fluid. Treatment with intravenous acyclovir (three cases) and intravenous ganciclovir (one case), which resulted in resolution of all symptoms except blindness in one patient. Antibodies to VZV in the cerebrospinal fluid of HIV-positive individuals may allow early diagnosis and lifesaving treatment of VZV meningoencephalitis.

Comparison of Tzanck smear, viral culture, and DNA diagnostic methods in detection of herpes simplex and varicella-zoster infection

<h3>Objective.</h3> —To compare Tzanck smears, viral cultures, and DNA diagnostic methods using the polymerase chain reaction (PCR) in detection of herpes simplex virus (HSV) or varicella-zoster virus (VZV) infection in clinically suspected cases. <h3>Design.</h3> —A 12-month trial comparing PCR with viral cultures and Tzanck smears in patients with clinically suspected HSV or VZV infection. <h3>Setting.</h3> —Both ambulatory and hospitalized patients were recruited from a tertiary referral center and the Miami (Fla) Veterans Affairs Medical Center. <h3>Patients.</h3> —Convenience samples of patients clinically suspected to have HSV (n=48) or VZV (n=35). To be included in the final analysis patients needed to have a positive Tzanck smear, viral culture, or PCR result. Patients who were clinically suspected to have HSV but had VZV by viral culture or PCR were analyzed in the VZV group. Similarly, patients who were clinically suspected to have VZV, but had HSV by viral culture or PCR were analyzed in the HSV group. Seventy-seven patients were available for final analysis: HSV (n=30), VZV (n=32), and 15 control cases who did not have evidence of viral infection. <h3>Results.</h3> —For HSV, PCR detected HSV DNA sequences in 73% of stained smears and 83% of unstained smears. For VZV infection, VZV DNA sequences were detected in 88% of stained smears and 97% of unstained smears. Viral DNA sequences were not detected in the 15 control cases. Viral cultures were positive in 83% and 44% of HSV and VZV cases, respectively. The Tzanck smear was positive in 60% and 75% of HSV and VZV cases, respectively. <h3>Conclusions.</h3> —PCR is a reliable method for detecting HSV and VZV DNA sequences from single stained and unstained Tzanck smears. It is clearly superior to viral culture in identifying VZV infection and is equivalent to conventional culture techniques in identifying cases of HSV. (<i>JAMA</i>. 1992;268:2541-2544)

Comparison of Tzanck Smear, Viral Culture, and DNA Diagnostic Methods in Detection of Herpes Simplex and Varicella-Zoster Infection

To compare Tzanck smears, viral cultures, and DNA diagnostic methods using the polymerase chain reaction (PCR) in detection of herpes simplex virus (HSV) or varicella-zoster virus (VZV) infection in clinically suspected cases. A 12-month trial comparing PCR with viral cultures and Tzanck smears in patients with clinically suspected HSV or VZV infection. Both ambulatory and hospitalized patients were recruited from a tertiary referral center and the Miami (Fla) Veterans Affairs Medical Center. Convenience samples of patients clinically suspected to have HSV (n = 48) or VZV (n = 35). To be included in the final analysis patients needed to have a positive Tzanck smear, viral culture, or PCR result. Patients who were clinically suspected to have HSV but had VZV by viral culture or PCR were analyzed in the VZV group. Similarly, patients who were clinically suspected to have VZV, but had HSV by viral culture or PCR were analyzed in the HSV group. Seventy-seven patients were available for final analysis: HSV (n = 30), VZV (n = 32), and 15 control cases who did not have evidence of viral infection. For HSV, PCR detected HSV DNA sequences in 73% of stained smears and 83% of unstained smears. For VZV infection, VZV DNA sequences were detected in 88% of stained smears and 97% of unstained smears. Viral DNA sequences were not detected in the 15 control cases. Viral cultures were positive in 83% and 44% of HSV and VZV cases, respectively. The Tzanck smear was positive in 60% and 75% of HSV and VZV cases, respectively. PCR is a reliable method for detecting HSV and VZV DNA sequences from single stained and unstained Tzanck smears. It is clearly superior to viral culture in identifying VZV infection and is equivalent to conventional culture techniques in identifying cases of HSV.

Studies on the pathogenesis of neurological diseases associated with Varicella‐Zoster Virus

Immunocytochemical techniques and in situ hybridization with three different Varicella-Zoster Virus (VZV)-specific RNA probes have been used to study the pathogenesis of VZV-associated neurological syndromes. Varicella-Zoster Virus antigens were not detected using the avidin-biotin peroxidase technique with a polyvalent anti-VZV antibody in any of the formalin-fixed tissue sections from eight cases of VZV-associated neurological disease (encephalitis, myelitis, ganglionitis); one case was immunosuppressed although inflammatory lesions were present. Intense labelling was detected within the inflammatory lesions in several representative VZV cases with a monoclonal antibody against Class II MHC antigens, whereas cases of Herpes Simplex Virus encephalitis and normal controls were not so labelled. Three VZV probes from open reading frames 62, 16 and 40, which show homology with the Herpes Simplex Virus immediate early 175 kd protein, the 65 kd DNA binding protein and the major capsid protein respectively, were used for in situ hybridization studies in these VZV tissues. Although the probes were able to detect VZV RNA in VZV-infected CV-1 and Flow 2002 cell cultures and formalin-fixed VZV skin biopsy sections, positive hybridization was not seen in any of the neurological cases studied. Thus neither VZV nucleic acid nor antigens were detected in any of the cases of VZV-associated neurological disease. It is proposed that the mechanism of neurological damage in the syndromes is immune-mediated, there being increased expression of Class II MHC antigens associated with persistent inflammation.