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Biomedical subjects

A Arvin

Publications and source records attributed to A Arvin.

At least 19 recordsLinked to original sources
PubMed2005

Frostbite: incidence and predisposing factors in mountaineers.

BACKGROUND: Frostbite, the most common cold injury, occurs in mountaineers, a major group at risk, more often than in the general population. OBJECTIVES: To describe the incidence of frostbite and the situations associated with it in mountaineering, emphasising factors that can be modified to decrease its frequency and severity. METHODS: In this cross sectional, questionnaire based study, 637 mountaineers were asked if they had suffered any frostbite injuries during the preceding two years and to provide the personal and circumstantial details. RESULTS: The mean incidence was 366/1000 population per year. Grade 1 injury (83.0%) and hands (26.4%) and feet (24.1%) involvement were most common. There was a significant relation between lack of proper equipment (odds ratio 14.3) or guide (p<0.001) and the injury. Inappropriate clothing, lack or incorrect use of equipment, and lack of knowledge of how to deal with cold and severe weather were claimed to be the main reasons for the injury. CONCLUSIONS: In high altitude and winter expeditions, mountaineers should wear appropriate clothing, have the necessary equipment such as quality boots and mittens, use a competent guide, and have training on how to tackle cold weather. They should also avoid wet clothing, windy terrains, and should never remain in the same position for long periods to reduce the risk of cold injuries.

Adolescent↗
PubMed2001

Immune evasion mechanisms of varicella-zoster virus.

Varicella-zoster virus can to modulate the expression of class I and class II major histocompatibility (MHC) molecules. MHC class I expression is downregulated in VZV-infected T cells as well as in fibroblasts. VZV-infected cells do not respond to exposure to interferon-gamma (IFN-gamma) by upregulation of MHC class II expression. However, MHC class II expression is induced when cells are treated with IFN-gamma before VZV infection. These effects on MHC class I and class II expression can be expected to interfere transiently with adaptive immune responses of the host, mediated by CD4 and CD8 T cells, ensuring that the virus has sufficient opportunity for transmission to susceptible contracts.

Animals↗
PubMed2000

Genotypic stability of cold-adapted influenza virus vaccine in an efficacy clinical trial.

An investigational live influenza virus vaccine, FluMist, contains three cold-adapted H1N1, H3N2, and B influenza viruses. The vaccine viruses are 6/2 reassortants, in which the hemagglutinin (HA) and neuraminidase (NA) genes are derived from the circulating wild-type viruses and the remaining six genes are derived from the cold-adapted master donor strains. The six genes from the cold-adapted master donor strains ensure the attenuation, and the HA and NA genes from the wild-type viruses confer the ability to induce protective immunity against contemporary influenza strains. The genotypic stability of this vaccine was studied by employing clinical samples collected during an efficacy trial. Viruses present in the nasal and throat swab specimens and in supernatants after culturing the specimens were detected and subtyped by multiplex reverse transcriptase (RT)-PCR. Complete genotypes of these detected viruses were determined by a combination of RT-PCR and restriction fragment length polymorphism, multiplex RT-PCR and fluorescent single-strand conformation polymorphism, and nucleic acid sequencing analysis. The FluMist vaccine appeared to be genotypically stable after replication in the human host. All viruses detected during the 2-week postvaccination period were shed vaccine viruses and had maintained the 6/2 genotype.

Cold Temperature↗
PubMed1999

Varicella-zoster virus immune evasion.

CD4+ and CD8+ T cells play dual roles in varicella-zoster virus (VZV) pathogenesis. The first role is to deliver the virus to cutaneous sites during primary VZV infection, permitting replication at these sites and the successful transmission of the virus to other susceptible individuals. The second contribution of T cells is to provide the critical antigen-specific adaptive immunity needed to stop viral replication and maintain VZV latency in sensory ganglia. The equilibrium between VZV and the host can be predicted to be served by immune evasion mechanisms in at least two important ways, including the facilitation of cell-associated viremia during primary VZV infection and silent persistence in dorsal root ganglia. Interference with antigen presentation by MHC class I downregulation may be expected to play a role in both circumstances. Transient interference with MHC class II expression in varicella skin lesions should facilitate local replication and transmission. In addition, when VZV reactivates, the capacity of viral gene products to block the upregulation of MHC class II expression triggered by interferon-gamma should permit a sufficient period of viral replication to cause the lesions of herpes zoster, despite the presence of VZV-specific T cells, and to allow transmission of the virus to susceptible individuals. Although the effort is at an early stage compared to studies of other viral pathogens, identifying the VZV gene products that exert these effects and their mechanisms of interference has the potential to reveal novel aspects of MHC class I and class II antigen processing and presentation.

Animals↗
PubMed1999

Characterization of Varicella-Zoster virus glycoprotein K (open reading frame 5) and its role in virus growth.

Varicella-zoster virus (VZV) is an alphaherpesvirus that is the causative agent of chickenpox and herpes zoster. VZV open reading frame 5 (ORF5) encodes glycoprotein K (gK), which is conserved among alphaherpesviruses. While VZV gK has not been characterized, and its role in viral replication is unknown, homologs of VZV gK in herpes simplex virus type 1 (HSV-1) and pseudorabies virus (PRV) have been well studied. To identify the VZV ORF5 gene product, we raised a polyclonal antibody against a fusion protein of ORF5 codons 25 to 122 with glutathione S-transferase and used it to study the protein in infected cells. A 40,000-molecular-weight protein was detected in cell-free virus by Western blotting. In immunogold electron microscopic studies, VZV gK was in enveloped virions and was evenly distributed in the cytoplasm in infected cells. To determine the function of VZV gK in virus growth, a series of gK deletion mutants were constructed with VZV cosmid DNA derived from the Oka strain. Full and partial deletions in gK prevented viral replication when the gK mutant cosmids were transfected into melanoma cells. Insertion of the HSV-1 (KOS) gK gene into the endogenous VZV gK site did not compensate for the deletion of VZV gK. The replacement of VZV gK at a nonnative AvrII site in the VZV genome restored the phenotypic characteristics of intact recombinant Oka (rOka) virus. Moreover, gK complementing cells transfected with a full gK deletion mutant exhibited viral plaques indistinguishable from those of rOka. Our results are consistent with the studies of gK proteins of HSV-1 and PRV showing that gK is indispensable for viral replication.

Amino Acid Sequence↗
PubMed1998

Polymerase chain reaction and restriction fragment length polymorphism analysis of varicella-zoster virus isolates from the United States and other parts of the world.

A polymerase chain reaction (PCR) assay that identifies and differentiates wild-type (wt) and vaccine strains of varicella-zoster virus (VZV) was used to determine if VZV strains with restriction fragment length polymorphisms resembling those of the Japanese Oka vaccine strain were present in the wt pool outside of Japan. Virus samples (n = 114) from patients with chickenpox and zoster from various parts of the United States and Australia were analyzed. The assay correctly identified 113 samples as wt strain. The 1 sample identified as Oka vaccine strain came from a child with leukemia who developed a vaccine-associated rash after receiving the live attenuated varicella vaccine. At this point, there is no evidence that wt strains resembling the vaccine are circulating outside of Japan. This indicates that this PCR assay can be utilized to distinguish rashes due to vaccine and wt VZV.

Australia↗
PubMed1996

Administration of oral acyclovir suppressive therapy after neonatal herpes simplex virus disease limited to the skin, eyes and mouth: results of a phase I/II trial.

BACKGROUND: Neonatal herpes simplex virus (HSV) infections limited to the skin, eyes and mouth (SEM) can result in neurologic impairment. A direct correlation exists between the development of neurologic deficits and the frequency of cutaneous HSV recurrences. Thus, the National Institutes of Allergy and Infectious Diseases Collaborative Antiviral Study Group conducted a Phase I/II trial of oral acyclovir therapy for the suppression of cutaneous recurrences after SEM disease in 26 neonates. METHODS: Infants < or = 1 month of age with virologically confirmed HSV-2 SEM disease were eligible for enrollment. Suppressive oral acyclovir therapy (300 mg/m2/dose given either twice daily or three times per day) was administered for 6 months. RESULTS: Twelve (46%) of the 26 infants developed neutropenia (< 1000 cells/mm3) while receiving acyclovir. Thirteen (81%) of the 16 infants who received drug 3 times per day experienced no recurrences of skin lesions while receiving therapy. In comparison, a previous Collaborative Antiviral Study Group study found that only 54% of infants have no cutaneous recurrences in the 6 months after resolution of neonatal HSV disease if oral acyclovir suppressive therapy is not initiated. In one infant, HSV DNA was detected in the cerebrospinal fluid during a cutaneous recurrence, and an acyclovir-resistant HSV mutant was isolated from another patient during the course of the study. CONCLUSIONS: Administration of oral acyclovir can prevent cutaneous recurrences of HSV after neonatal SEM disease. The effect of such therapy on neurologic outcome must be assessed in a larger, Phase III study. As such, additional investigation is necessary before routine use of suppressive therapy in this population can be recommended.

Acyclovir↗
PubMed1995

Safety and cellular and humoral immune responses of a booster dose of varicella vaccine 6 years after primary immunization.

Four hundred nineteen children and adolescents immunized with live varicella vaccine 4-6 years earlier were enrolled in a study to evaluate the safety and immune response to a booster dose containing approximately 3300 pfu of virus. Of the subjects, 99% (414/419) maintained antibody to varicella zoster virus (VZV) with a geometric mean titer of 25.7 and mean stimulation index (SI) for VZV-specific lymphoproliferation response of 40.3 +/- 5.3 (SE). Some 7-10 days after the booster immunization, seropositivity rates increased to 100% (302/302), and GMT was 143.6 (anamnestic response). At 6 weeks after the booster inoculation, a subset of subjects had 100% seropositivity (74/74) with a GMT of 218.8 and an SI of 58.6. After 3 months, seropositivity was 100% (358/358), GMT was 119.0, and SI was 61.4.

Adolescent↗
PubMed1992

Comparison of the Western immunoblot assay and a glycoprotein G enzyme immunoassay for detection of serum antibodies to herpes simplex virus type 2 in patients with AIDS.

Herpes simplex virus type 2 (HSV-2) seroprevalence in 68 patients with AIDS was 77% by Western blot (immunoblot) and 44% by glycoprotein G-2 immunoassay. Each of 16 patients with culture-proven HSV-2 infection was positive by Western blot versus 8 by glycoprotein G-2 immunoassay. No differences in age, race, duration of AIDS, acyclovir usage, or HSV-1 seroprevalence were found to explain differences in sensitivity.

Acquired Immunodeficiency Syndrome↗
PubMed1991

A controlled trial comparing vidarabine with acyclovir in neonatal herpes simplex virus infection. Infectious Diseases Collaborative Antiviral Study Group.

BACKGROUND: Despite the use of vidarabine, herpes simplex virus (HSV) infection in neonates continues to be a disease of high morbidity and mortality. We undertook a controlled trial comparing vidarabine with acyclovir for the treatment of neonatal HSV infection. METHODS: Babies less than one month of age with virologically confirmed HSV infection were randomly and blindly assigned to receive either intravenous vidarabine (30 mg per kilogram of body weight per day; n = 95) or acyclovir (30 mg per kilogram per day; n = 107) for 10 days. Actuarial rates of mortality and morbidity among the survivors after one year were compared overall and according to the extent of the disease at entry into the study (infection confined to the skin, eyes, or mouth; encephalitis; or disseminated disease). RESULTS: After adjustment for differences between groups in the extent of disease, there was no difference between vidarabine and acyclovir in either morbidity (P = 0.83) or mortality (P = 0.27). None of the 85 babies with disease confined to the skin, eyes, or mouth died. Of the 31 babies in this group who were treated with vidarabine and followed for a year, 88 percent (22 of 25) were judged to be developing normally after one year, as compared with 98 percent (45 of 46) of the 54 treated with acyclovir (95 percent confidence interval for the difference, -4 to 24). For the 71 babies with encephalitis, mortality was 14 percent with vidarabine (5 of 36) and with acyclovir (5 of 35); of the survivors, 43 percent (13 of 30) and 29 percent (8 of 28), respectively, were developing normally after one year (95 percent confidence interval for the difference, -11 to 39). For the 46 babies with disseminated disease, mortality was 50 percent (14 of 28) with vidarabine and 61 percent (11 of 18) with acyclovir (95 percent confidence interval for the difference, -20 to 40); of the survivors, 58 percent (7 of 12) and 60 percent (3 of 5), respectively, were judged to be developing normally after one year (95 percent confidence interval for the difference, -40 to 50). Both medications were without serious toxic effects. CONCLUSIONS: In this multicenter, randomized, blinded study there were no differences in outcome between vidarabine and acyclovir in the treatment of neonatal HSV infection. The study lacked statistical power to determine whether there were sizable differences within the subgroups of those with localized HSV, encephalitis, or disseminated disease.

Acyclovir↗
PubMed1991

Predictors of morbidity and mortality in neonates with herpes simplex virus infections. The National Institute of Allergy and Infectious Diseases Collaborative Antiviral Study Group.

BACKGROUND: In a controlled trial comparing acyclovir with vidarabine in the treatment of neonatal herpes simplex virus (HSV) infection, we found no significant difference between the treatments in adjusted mortality and morbidity. Hence, we sought to define for the entire cohort (n = 202) the clinical characteristics that best predicted the eventual outcome in these neonates. METHODS: Data were gathered prospectively at 27 centers between 1981 and 1988 in infants less than one month of age who had virologically confirmed HSV infection. We examined the outcomes by multivariate analyses of 24 variables. Disease was classified in one of three categories based on the extent of the involvement at entry into the trial: infection confined to skin, eyes, or mouth; encephalitis; or disseminated infection. RESULTS AND CONCLUSIONS: There were no deaths among the 85 infants with localized HSV infection. The mortality rate was significantly higher in the 46 neonates with disseminated infection (57 percent) than in the 71 with encephalitis (15 percent). In addition, the risk of death was increased in neonates who were in or near coma at entry (relative risk, 5.2), had disseminated intravascular coagulopathy (relative risk, 3.8), or were premature (relative risk, 3.7). In babies with disseminated disease, HSV pneumonitis was also associated with greater mortality (relative risk, 3.6). In the survivors, morbidity was most frequent in infants with encephalitis (relative risk, 4.4), disseminated infection (relative risk, 2.1), seizures (relative risk, 3.0), or infection with HSV type 2 (relative risk, 4.9). With HSV infection limited to the skin, eyes, or mouth, the presence of three or more recurrences of vesicles was associated with an increased risk of neurologic impairment as compared with two or fewer recurrences.

Consciousness↗
PubMed1988

Changing presentation of herpes simplex virus infection in neonates.

We compared the clinical presentation of 95 newborns with herpes simplex virus (HSV) infection from 1973 through 1981 (first period) with data from 196 newborns evaluated from 1982 through 1987 (second period). There was a significant change in the presentation of infection in these infants. From the first to the second period, the frequency of disseminated disease decreased from 50.5% to 22.9%, whereas the frequency of skin, eye, and mouth (SEM) diseases increased from 17.9% to 43.4% (P less than .001). The frequency of infants with central nervous system (CNS) disease remained relatively unchanged--31.6% versus 33.7%. We also compared the demographic and clinical characteristics of the infants and their mothers. For neonates with CNS or disseminated infection, disease duration and frequency of prematurity were significantly decreased in the second period, as was the frequency of skin vesicles for newborns with SEM or disseminated infection. These changes are most likely the consequence of recognizing and treating SEM infection before its progression to more-severe disease.

Central Nervous System↗
PubMed1987

Intrauterine herpes simplex virus infections.

Neonatal herpes simplex virus (HSV) infection is usually acquired at birth, although a few infants have had findings suggestive of intrauterine infection. We describe 13 babies who had clinical manifestations of intrauterine HSV infection, including skin lesions and scars at birth (12), chorioretinitis (eight), microcephaly (seven), hydranencephaly (five), and microphthalmia (two). All infants had combinations of these defects. Infection was proved by viral isolation in each case; all isolates were HSV-2. Two infants died during the first week of life; 10 of the surviving infants had severe neurologic sequelae, and one infant was blind. Four mothers experienced an apparent primary genital HSV infection, and one had recurrent infection, at varying times during gestation. The remaining women denied a history of symptoms of genital HSV infection. These findings indicate that intrauterine HSV infection can occur as a consequence of either primary or recurrent maternal infection and has severe consequences for the fetus.

Abnormalities, Multiple↗
PubMed1987

Giant cell pneumonia caused by parainfluenza type 3 in a patient with acute myelomonocytic leukemia.

A 4 1/2-year-old boy with acute myelomonocytic leukemia developed fever, neutropenia, and a prolonged respiratory illness while receiving maintenance chemotherapy. An open lung biopsy specimen demonstrated a giant cell pneumonia with intracytoplasmic and probable intranuclear viral inclusions of the paramyxovirus type. Serologic studies demonstrated convincing evidence of a parainfluenza type 3 infection. Although parainfluenza type 3-induced giant cell pneumonia has been reported in infants with the severe combined immunodeficiency syndrome, to our knowledge, this is the first reported case of this complication in a patient with leukemia.

Child, Preschool↗
PubMed1986

Chronic infectious mononucleosis syndrome, pancytopenia, and polyclonal B-lymphoproliferation terminating in acute lymphoblastic leukemia.

A 17-year-old previously healthy girl is reported who developed acute infectious mononucleosis followed by progressive ill health over 20 months, associated with pancytopenia and a polyclonal B-lymphoproliferation, terminating in acute lymphoblastic leukemia (ALL). Epstein-Barr virus (EBV) was recovered from the patient's nasopharyngeal secretions; serologic titers of antibodies to EBV-associated antigens were compatible with a chronic persistent EBV infection. Plasma interferon levels were markedly elevated. EBV-specific cell-mediated immunity, as well as Natural killer (NK) cell activity were markedly deficient. Other studies of cell-mediated immunity revealed notable abnormalities, including abnormalities in T-cell subset ratios, and a serum blocker of autologous mitogen-induced lymphoproliferation. Humoral (plasma)-mediated, but not cell-mediated, suppression of hemopoiesis was demonstrated using in vitro erythroid and myeloid colony culture techniques. Immunophenotyping of the patient's bone marrow cells preterminally was consistent with ALL. Autopsy revealed pathologic changes of ALL in marrow and multiple organs. We conclude that our patient developed an EBV-driven lymphoproliferative disorder, with associated defective cell-mediated immunity and hemopoiesis. Ultimately, the patient's documented polyclonal lymphoproliferative state was superimposed by acute lymphoblastic leukemia.

Adolescent↗
PubMed1982

Effects of interferon-alpha on human warts.

Two patients with extensive warts which were stable for two years or more were treated with human interferon-alpha to assess the ability of interferon to affect this benign tumor of viral etiology. Intramuscular administration of 96.6 and 135 million units over 12-15 weeks produced softening and decreased scaling of each patient's warts. Double blind, placebo-controlled intralesional injections resulted in progressive disappearance of interferon treated warts. A dose response relationship was shown in eight warts. The minimum effective dose was 1.2 x 10(6) units injected over 15.5 weeks.

Adult↗