Vgv virus

A second sample should be collected and tested. A positive result indicates exposure to the pathogen or administration of specific immunoglobulins. It is not an indication of active infection or stage of disease. A primary Herpes simplex infection can stimulate a heterologous antibody response in individuals previously infected by VZV. The absence of a significant antibody rise does not necessarily rule out VZV infection.

The performance characteristics of this test have not been established for CSF, neonates, infants or cord blood. This is a qualitative test; quantitation for comparison of acute and convalescent sera has not been validated by the manufacturer of the current test system.

Result values from different methodologies or from different institutions cannot be compared. Timing of specimen collection for paired sera is critical. In some patients, antibody may rise to significant levels and fall again to lower or undetectable levels within a month.

Other patients may not develop significant antibody levels. Med J Aust. Herpes zoster with dysfunction of bladder and anus. Neurological picture. Findings of segmental zoster paresis on MRI. J Neurol Neurosurg Psychiatry. Brachial plexopathy following herpes zoster infection: two cases with MRI findings. J Neurol Sci. Segmental zoster paresis — a disease profile. Smith FP. Pathological studies of spinal nerve ganglia in relation to intractable intercostal pain.

Surg Neurol. The prognosis with postherpetic neuralgia. Voltage-gated sodium channels and hyperalgesia. Annu Rev Pharmacol Toxicol. Kennedy PGE, et al. Varicella-zoster viruses associated with post-herpetic neuralgia induce sodium current density increases in the ND Nav Persistence of varicella-zoster virus DNA in elderly patients with postherpetic neuralgia. Chronic varicella-zoster virus ganglionitis — a possible cause of postherpetic neuralgia.

Valaciclovir compared with acyclovir for improved therapy for herpes zoster in immunocompetent adults. Antimicrob Agents Chemother. Degreef H. Famciclovir, a new oral antiherpes drug: results of the first controlled clinical study demonstrating its efficacy and safety in the treatment of uncomplicated herpes zoster in immunocompetent patients.

Int J Antimicrob Agents. Acyclovir for treatment of postherpetic neuralgia: efficacy and pharmacokinetics. Improvement of postherpetic neuralgia after treatment with intravenous acyclovir followed by oral valacyclovir. Arch Neurol. Chen N, et al. Antiviral treatment for preventing postherpetic neuralgia. Cochrane Database Syst Rev. Postherpetic neuralgia.

Varicella-zoster virus meningoencephalitis in an immunocompetent patient without a rash. Scand J Infect Dis. A woman with acute headache and sacral dermatomal numbness. Varicella zoster virus cerebellitis in a year-old patient without herpes zoster. Ciccone S, et al. Stroke after varicella-zoster infection: report of a case and review of the literature. Increased risk of stroke after a herpes zoster attack: a population-based follow-up study. Nagel MA, et al.

The varicella zoster virus vasculopathies: clinical, CSF, imaging, and virologic features. This paper demonstrates that VZV vasculopathies in cerebral arteries lead to strokes. Herpes zoster ophthalmicus and the risk of stroke: a population-based follow-up study. Herpes zoster ophthalmicus and delayed contralateral hemiparesis caused by cerebral angiitis: diagnosis and management approaches. Herpes zoster ophthalmicus and delayed ipsilateral cerebral infarction. This paper shows the link between VZV infection and stroke.

Varicella zoster virus vasculopathy: analysis of virus-infected arteries. Varicella zoster virus vasculopathies: diverse clinical manifestations, laboratory features, pathogenesis, and treatment. Lancet Neurol. Grose C.

Stroke after varicella and zoster ophthalmicus: another indication for treatment and immunization. Gilden D, et al. Prevalence and distribution of VZV in temporal arteries of patients with giant cell arteritis. Franco-Paredes C, et al. Aseptic meningitis and optic neuritis preceding varicella-zoster progressive outer retinal necrosis in a patient with AIDS. Furuta Y, et al. Varicella-zoster virus reactivation is an important cause of acute peripheral facial paralysis in children.

Varicella zoster disease of the central nervous system: epidemiological, clinical, and laboratory features 10 years after the introduction of the varicella vaccine. This paper describes meningitis and encephalitis caused by VZV, often without rash. Varicella-zoster virus reactivation without rash. Gilden DH, et al. Varicella zoster virus, a cause of waxing and waning vasculitis: the New England Journal of Medicine case 5— revisited.

Varicella-zoster virus infections of the nervous system: clinical and pathologic correlates. Arch Pathol Lab Med. McKelvie PA, et al. Meningoencephalomyelitis with vasculitis due to varicella zoster virus: a case report and review of the literature. Risk of stroke following herpes zoster: a self-controlled case-series study. This paper provides further recognition of the relationship between VZV and stroke. Varicella-zoster virus myelitis: an expanding spectrum.

Chen JJ, et al. Latent, lytic and reactivating varicella zoster virus in the ENS of humans and guinea pigs: could intestinal shingles be a hidden cause of gastrointestinal disease? Neuroastroenterol Motil. Edelman DA, et al. Ogilvie syndrome and herpes zoster: case report and review of the literature. J Emerg Med. Acta Haematol. Use of saliva to identify varicella-zoster virus VZV infection of the gut.

This paper identifies VZV infection of the gastrointestinal tract in the absence of rash. Leung J, et al.

Evaluation of laboratory methods for diagnosis of varicella. Harbecke R, et al. A real-time PCR assay to identify and discriminate among wild-type and vaccine strains of varicella-zoster virus and herpes simplex virus in clinical specimens, and comparison with the clinical diagnoses. Mehta SK, et al. Rapid and sensitive detection of varicella zoster virus in saliva of patients with herpes zoster.

J Virol Methods. Varicella-zoster virus in the saliva of patients with herpes zoster. Quantitation of varicella-zoster virus DNA in patients with Ramsay Hunt syndrome and zoster sine herpete. J Clin Microbiol. Detection of varicella-zoster virus DNA by polymerase chain reaction in the cerebrospinal fluid of patients suffering from neurological complications associated with chicken pox or herpes zoster.

The effectiveness of the varicella vaccine in clinical practice. Resistance testing of clinical varicella-zoster virus strains.

Antiviral Res. Novel genetic variation identified at fixed loci in ORF62 of the Oka varicella vaccine and in a case of vaccine-associated herpes zoster.

This article describes the molecular differentiation between wild-type and vaccine-types of VZV using viral DNA from patients. LaRussa P, et al. Restriction fragment length polymorphism of polymerase chain reaction products from vaccine and wild-type varicella-zoster virus isolates.

Ibraheem M, et al. Fatal wild-type varicella-zoster virus encephalitis without a rash in a vaccinated child. National Health Service. Varicella Zoster Virus Reference Lab. Stress-induced subclinical reactivation of varicella zoster virus in astronauts. Papaevangelou V, et al. Subclinical VZV reactivation in immunocompetent children hospitalized in the ICU associated with prolonged fever duration.

Clin Microbiol Infect. Birlea M, et al. Search for varicella zoster virus DNA in saliva of healthy individuals aged 20—59 years. Live vaccine used to prevent the spread of varicella in children in hospital. This study describes the successful attenuation of VZV and the use of this live attenuated virus to prevent varicella, thereby demonstrating the first successful vaccine against varicella.

Gomi Y, et al. Comparison of the complete DNA sequences of the Oka varicella vaccine and its parental virus. Oxman MN. Zoster vaccine: current status and future prospects.

Yamanishi K. Molecular analysis of the Oka vaccine strain of varicella-zoster virus. This study identifies the molecular features of the attenuated vaccine strain of VZV compared with the wild-type strain. Peters GA, et al.

The attenuated genotype of varicella-zoster virus includes an ORF0 transitional stop codon mutation. Protection against varicella in family contacts by immediate inoculation with live varicella vaccine.

This is the first demonstration of the clinical effectiveness of the Oka strain in preventing varicella, together with immunological data. Asano Y, Takahashi M. Clinical and serologic testing of a live varicella vaccine and two-year follow-up for immunity of the vaccinated children. Live attenuated varicella vaccine. Efficacy for children with leukemia in remission. This paper provides the first proof that the varicella vaccine is safe and effective in preventing varicella in children with underlying leukaemia.

White CJ. Clinical trials of varicella vaccine in healthy children. Infect Dis Clin North Am. White CJ, et al. Weibel RE, et al. Live attenuated varicella virus vaccine. Efficacy trial in healthy children. This study demonstrates that varicella vaccination protects healthy children from chickenpox. Shapiro ED, et al. Effectiveness of 2 doses of varicella vaccine in children. Oral acyclovir prophylaxis of varicella after intimate contact.

Acyclovir prophylaxis of varicella after household exposure. A randomized, double-blind, placebo-controlled trial of valacyclovir prophylaxis to prevent zoster recurrence from months 4 to 24 after BMT. Bone Marrow Transplant. Ljungman P, et al. Long-term acyclovir prophylaxis in bone marrow transplant recipients and lymphocyte proliferation responses to herpes virus antigens in vitro.

Emergence of acyclovir-resistant varicella zoster virus in an AIDS patient on prolonged acyclovir therapy. Levin MJ, et al. Development of resistance to acyclovir during chronic infection with the Oka vaccine strain of varicella-zoster virus, in an immunosuppressed child. This paper demonstrates that VZV can reactivate in immunocompromised children and that the vaccine virus can become resistant to acyclovir.

Bhalla P, et al. Disseminated, persistent, and fatal infection due to the vaccine strain of varicella-zoster virus in an adult following stem cell transplantation.

Baxter R, et al. Long-term effectiveness of varicella vaccine: a year, prospective cohort study. Effectiveness over time of varicella vaccine. This study shows that immunity to varicella after vaccination does not wane substantially with time. Seward JF, et al. Varicella disease after introduction of varicella vaccine in the United States, — This study demonstrates personal and herd immunity as a result of vaccination in healthy children.

The protective effect of immunologic boosting against zoster: an analysis in leukemic children who were vaccinated against chickenpox. Varicella vaccination: impact of vaccine efficacy on the epidemiology of VZV. Exposure to varicella boosts immunity to herpes-zoster: implications for mass vaccination against chickenpox. The impact of the varicella vaccination program on herpes zoster epidemiology in the United States: a review.

Gaillat J, et al. This paper shows that immunity to VZV does not require continued exogenous exposure to VZV and that asymptomatic episodes of reactivation of VZV are likely to have a role in maintaining long-term immunity to the virus.

Contagiousness of varicella in vaccinated cases: a household contact study. Weinmann S, et al. Incidence and clinical characteristics of herpes zoster among children in the varicella vaccine era, — Galea SA, et al. The safety profile of varicella vaccine: a year review. Immunization to reduce the frequency and severity of herpes zoster and its complications. Elsevier; Vaccination against herpes zoster and postherpetic neuralgia. Schmader KE, et al. Effect of a zoster vaccine on herpes zoster-related interference with functional status and health-related quality-of-life measures in older adults.

J Am Geriatr Soc. Simberkoff MS, et al. Safety of herpes zoster vaccine in the shingles prevention study: a randomized trial. Tseng HF, et al. Herpes zoster vaccine in older adults and the risk of subsequent herpes zoster disease.

Herpes zoster vaccine effectiveness against incident herpes zoster and post-herpetic neuralgia in an older US population: a cohort study. PLoS Med. Efficacy, safety, and tolerability of herpes zoster vaccine in persons aged 50—59 years. Persistence of the efficacy of zoster vaccine in the shingles prevention study and the short-term persistence substudy. Morrison VA, et al. Long-term persistence of zoster vaccine efficacy. Berkowitz EM, et al.

Chlibek R, et al. Lal H, et al. Efficacy of an adjuvanted herpes zoster subunit vaccine in older adults. This is the first demonstration of an adjuvanted subunit vaccine that is not infectious can prevent zoster in the elderly. Cohen JIA. A new vaccine to prevent herpes zoster. Acyclovir for treating varicella in otherwise healthy children and adolescents. Belay ED, et al. Severe necrotizing soft-tissue infections and nonsteroidal anti-inflammatory drugs.

Clin Exp Dermatol. The use of oral acyclovir in otherwise healthy children with varicella. Feldman S, Lott L. Varicella in children with cancer: impact of antiviral therapy and prophylaxis.

Etzioni A, et al. Fatal varicella associated with selective natural killer cell deficiency. This study shows the importance of innate immunity in host defences against VZV. Acyclovir therapy of chickenpox in immunosuppressed children — a collaborative study. This is the first demonstration of successful antiviral therapy to protect immunocompromised children from varicella.

Treatment of adult varicella with oral acyclovir. A randomized, placebo-controlled trial. Balfour HH, et al. Controlled trial of acyclovir for chickenpox evaluating time of initiation and duration of therapy and viral resistance.

Sauerbrei A, Wutzler P. Herpes simplex and varicella-zoster virus infections during pregnancy: current concepts of prevention, diagnosis and therapy. Part 2: Varicella-zoster virus infections. Med Microbiol Immunol. In these cells, limited transcription may take place from some, but not all, of the immediate early and early genes of the latent viral genome.

Thus, expression of latent varicella-zoster virus genes appears to be different from that of HSVs. Where mainly non-polyadenylated LATs that are antisense to immediate early transcripts are expressed and accumulate in neuronal cells. VZV-encoded LATs are polyadenylated transcripts of the sense direction that have a short half-life and are detectable in non-neuronal, satellite cells and in ganglia as well. However, there is no significant viral protein synthesis detectable from the polyadenylated transcripts during latency.

The molecular basis of latency and reactivation of latent virus has not been fully characterized. Measles is normally an acute self-limited disease in which the virus appears to be eliminated. In rare individuals, however, virus persists in the brain despite apparent humoral and cellular immune responses. Possible mechanisms of persistence include the immunologically privileged status of the brain, antiviral antibody-induced internalization of viral antigens, altered and restricted virus expression and replication as a result of mutations in the virus genome.

This persistent virus infection is manifested by progressive mental deterioration, involuntary movements, muscular rigidity, and coma see Ch. The inability of measles virus to complete its replication cycle is associated with a variety of transcriptional and translational anomalies which affect the expression, stability, or function of the matrix M , fusion F and hemagglutinin H genes.

In affected neurons there is an accumulation of inclusion bodies containing nucleocapsids, and surface proteins H, F and M. Virus-infected cells may avoid immune surveillance by mutation in the M protein encoding gene that may explain restricted production and budding of virus and syncytia formation in SSPE, which favors persistence. SSPE patients have high titers of anti-measles antibodies in both serum and cerebrospinal fluid; however, antibody to M protein is often lacking.

BK virus has been associated with hemorrhagic cystitis; however, the site of persistence is not known. The JC virus is thought to persist in the kidney, and is reactivated when the host immune system is impaired e.

JC virus is regularly isolated from brain cells of patients with progressive multifocal leukoencephalopathy PML , a fatal demyelinating disease. The mechanism of persistence for both viruses can be related to the encoded T antigens, which are functionally similar, but antigenically distinct from SV40 T antigen.

The latent JC virus genome can randomly integrate into cellular DNA and, when excision of viral DNA is induced, the latent genome becomes activated, infectious virus is produced, and disease PML may develop.

The subacute spongiform virus encephalopathies are a unique type of slow virus infection caused by agents called unconventional viruses or prions see Ch. Many lines of evidence have converged to argue that these infectious agents are composed largely, if not entirely, of prion protein PrP molecules. These proteins are encoded by wild type or mutated cellular genes that are excluded from the particles. The human PrPs gene can be mapped to the short arm of chromosome A long incubation period often years to decades with slowly rising and spreading infection precedes the onset of clinical illness and is followed by chronic progressive disease.

The host shows no inflammatory response, no humoral or cellular immune response, and no interferon production. Immunosuppression of the host has no effect on pathogenesis or progression of disease.

The human subacute spongiform virus encephalopathies include kuru, Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker syndrome and fatal familial insomnia. Of the numerous viruses that infect the digestive system, most the enteroviruses and reoviruses are considered to be acute viruses that cause infections even though some may continue to be shed for months or even years.

Persistent infections may be caused by hepatitis viruses, adenoviruses, and parvoviruses Table Chronic hepatitis develops in about 10—15 percent of hepatitis B patients. The presence of viral surface antigen HBsAg or core antigen HbcAG in serum serves as a marker of persistent infection.

In chronic infections, HBV productively infects hepatocytes and maintains a low level of virus production over a long period. Integration is not required for virus replication, but it may be a crucial event for long-term perpetuation of the virus genome. In addition, HBV is capable of causing latent infections e. The factors that determine the development of chronic infection with HBV have not been fully identified.

Immune tolerance to the surface protein of HBV appears to be one of the factors involved in the development of the carrier state. The chronic infection is related to an inefficient T-cell response to viral components critical for protective immunity.

There is strong epidemiological evidence of a causal relationship between persistent HBV infection and development of hepatocellular carcinoma. Individuals who have antibody to hepatitis C should be considered potentially persistently infected, and the presence of viral RNA in infections by hepatitis C are associated with chronic persistent or active hepatitis, cirrhosis, and hepatocellular carcinoma.

The mechanism of this interaction is currently being studied. There is no evidence that hepatitis A or E causes persistent infections.

Adenoviruses AdV typically cause acute disease of the respiratory and gastrointestinal tracts of human beings. The high incidence of adenovirus infections in organ transplant kidney, bone marrow recipients and AIDS patients suggests that these infections most probably represent reactivation of a latent adenovirus infection.

For example, AdV can persist latently for years in adenoids and tonsils and often are shed in the feces for many months after the initial infection.

The mechanism and the cell type harboring the latent virus in vivo is presently unknown. In vitro studies have shown that the strategies of C-type AdV types AdV2, AdV5 to evade immune recognition involve the e 3 early genomic region. Protein s of the e 3 region alter the expression, post-translational modification and transport of the major histocompatibility complex HLA class I.

In addition, E3 down-regulates the e 1 a gene product, the immunodominant cytotoxic T cell determinant. It is possible that similar mechanisms operate in the host during natural persistent infection. The replication of the simplest DNA viruses, the parvoviruses, is dependent on functions supplied by replicating host cells Parvovirus genus or by coinfection with helper viruses, usually adenovirus Dependovirus genus. Both genuses have been shown to develop persistent infection in humans.

For example, parvovirus B19 infects primarily the erythroid progenitors, causing chronic hemolytic anemia, neutropenia, and persistent arthritis mainly in immunocompromised individuals. The dependovirus group of parvoviruses adeno-associated viruses; AAV can be isolated from fecal, ocular, or respiratory specimens and from penile and condylomatous lesions during simultaneous adenovirus infections.

The AAV integrate into host cell DNA and replicate with it, only to be excised and induced to replicate when the latently infected cells are superinfected with adenoviruses.

The dependoviruses are not known to be pathogenic. Of the viruses that cause acute infections of the skin and mucous membranes, herpesviruses see above and papillomaviruses Table are also capable of establishing persistent infections.

The ubiquity of latent papillomavirus infections is emphasized by the frequent, often acute outbreak of warts in immunosuppressed patients and pregnant women. HPVs specifically infect basal or germ cells of the epidermis. The virus genome persists in episomal form, as a result of the multiple DNA-protein and protein-protein interactions between viral and cellular regulatory factors. In latency, viral DNA replication and transcription are maintained at very low levels and regulated by negative cellular factors e.

For example, the viral E1 replication protein functions as an E2 co-repressor when bound to the origin of DNA replication. Productive viral replication occurs only in terminally-differentiated skin cells see Fig. Where, presumably in response to differentiation-specific signals, viral transcription accelerates, DNA synthesis begins and virions assemble see Ch. Persistent HPV infections are associated with a number of skin and cervical cancers see Ch.

The results are summarized below:. Sensitivity: Specificity: Overall percent agreement: Yankowitz J, Grose C: Congenital infections. In: Storch GA, ed. Essentials of diagnostic virology.

Churchill Livingstone; N Engl J Med. Med Pregl. Elsevier; Immunoglobulin M:. The presence or absence of IgM-class antibody to varicella-zoster virus VZV is determined by an indirect immunofluorescence assay. Serum is incubated with VZV antigen that is adhered to a glass microscope slide.

Antibodies, if present, will bind to the antigen forming stable antigen-antibody complexes. If no antibodies are present, the complexes will not be formed and the serum components will be washed away. Fluorescein-labeled antihuman-IgM antibody is added to the reaction side and binds to IgM antibodies, if present. This results in a positive reaction of bright apple-green fluorescence when viewed with a fluorescence microscope. Immunoglobulin G:.

Briefly, serum samples are mixed and incubated at 37 degrees C with sample diluent and dyed beads coated with VZV antigen. After a wash cycle, antihuman IgG antibody conjugated to phycoerythrin PE is added to the mixture and incubated at 37 degrees C. Excess conjugate is removed in another wash cycle and the beads are resuspended in wash buffer.

The bead mixture then passes through a detector that identifies the bead based on dye fluorescence and determines the amount of antibody captured by the antigen based on the fluorescence of the attached PE.

Raw data is calculated in relative fluorescence intensity. Three additional dyed beads, an internal standard bead, a serum verification bead, and a reagent blank bead are present in each reaction mixture to verify detector response, the addition of serum to the reaction vessel and the absence of significant nonspecific binding in serum. Monday through Saturday.