Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gianotti-Crosti syndrome (GCS), a self-limiting papulovesicular acrodermatitis often associated with underlying viral infection, is mainly described in children. Nine children with GCS were evaluated with dermatologic examination and serologic tests for viral infections. Therapy was modified according to the subjective symptoms of patients, which included characteristic acrolocated papulovesicles, generalized skin eruption, and mild to severe pruritus. Results of serologic investigations revealed Epstein-Barr virus, Coxsackie A virus, parvovirus B19, and parainfluenza virus 1/2. In three children no underlying viral infection was found. Therapeutic interventions included topical clioquinol lotion 1 percent, topical application of corticosteroids, systemic antihistaminic therapy, and systemic methylprednisolone. Skin lesions resolved after 2 to 4 weeks in treated as well as in nontreated children. Although GCS in children often lacks close association with a causative viral infection, such severe infections as hepatitis B and human immunodeficiency virus must be considered. Whole-body involvement seems to correlate with severe pruritus and additional general symptoms requiring more intensive therapy.
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PMID:Gianotti-Crosti syndrome: clinical, serologic, and therapeutic data from nine children. 987 81

A human immunodeficiency virus (HIV)-infected individual was first diagnosed with red blood cell aplasia due to B19 parvovirus infection in late 1989. Over the subsequent seven-year period, he received a total of 119 units of red blood cells (RBCs) and intravenous immunoglobulin every 2-3 weeks. In 1996 combination antiretroviral treatment with a protease inhibitor was initiated. He received four more units during the following two months and then required no more transfusions for the subsequent 24 months of follow-up. His CD4 count progressively increased and DNA polymerase chain reaction for parvovirus B19 became undetectable. Aggressive antiretroviral treatment may effectively diminish transfusion requirements among HIV-infected individuals with pure RBC aplasia resulting from parvovirus B19 infection.
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PMID:Persistent parvovirus B19 related anemia of seven years' duration in an HIV-infected patient: complete remission associated with highly active antiretroviral therapy. 992 13

Infections caused by human parvovirus B19 are known to be controlled mainly by neutralizing antibodies. To analyze the immune reaction against parvovirus B19 proteins, four cell lines secreting human immunoglobulin G monoclonal antibodies (MAbs) were generated from two healthy donors and one human immunodeficiency virus type 1-seropositive individual with high serum titers against parvovirus. One MAb is specific for nonstructural protein NS1 (MAb 1424), two MAbs are specific for the unique region of minor capsid protein VP1 (MAbs 1418-1 and 1418-16), and one MAb is directed to major capsid protein VP2 (MAb 860-55D). Two MAbs, 1418-1 and 1418-16, which were generated from the same individual have identity in the cDNA sequences encoding the variable domains, with the exception of four base pairs resulting in only one amino acid change in the light chain. The NS1- and VP1-specific MAbs interact with linear epitopes, whereas the recognized epitope in VP2 is conformational. The MAbs specific for the structural proteins display strong virus-neutralizing activity. The VP1- and VP2-specific MAbs have the capacity to neutralize 50% of infectious parvovirus B19 in vitro at 0.08 and 0.73 microgram/ml, respectively, demonstrating the importance of such antibodies in the clearance of B19 viremia. The NS1-specific MAb mediated weak neutralizing activity and required 47.7 micrograms/ml for 50% neutralization. The human MAbs with potent neutralizing activity could be used for immunotherapy of chronically B19 virus-infected individuals and acutely infected pregnant women. Furthermore, the knowledge gained regarding epitopes which induce strongly neutralizing antibodies may be important for vaccine development.
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PMID:Generation of neutralizing human monoclonal antibodies against parvovirus B19 proteins. 997 77

Parvovirus B19 causes persistent erythroid aplasia in immunocompromised hosts. From April through July 1996, we encountered five adult patients presenting with reticulocytopenia and fever caused by parvovirus B19 infection. The reticulocyte count of four patients with normal immunity recovered within two weeks after the onset of fever. However, in the one remaining patient with common variable immunodeficiency (CVI), reticulocytopenia, and other symptoms including fever and the elevation of lactate dehydrogenase (LDH) levels persisted beyond 16 days of onset. Although the DNA of parvovirus B19 was detected in the peripheral blood of the CVI patient, neither immunoglobulin Ig-G nor Ig-M antibodies specific to the virus were detectable. We administered 50 mg/kg of Ig to the CVI patient for six days. The reticulocyte count recovered promptly on the sixth day of the treatment and parvovirus B19 DNA was not detectable 30 days after therapy. This indicates that although patients with CVI may be susceptible to persistent erythroid aplasia during an endemic of parvovirus B19, the complication can be treated successfully with relatively low-dose Ig.
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PMID:Successful treatment of persistent erythroid aplasia caused by parvovirus B19 infection in a patient with common variable immunodeficiency with low-dose immunoglobulin. 1007 14

To determine the efficacy of a clean-in-place system for the inactivation of viruses present in human plasma, the effect of 0.1 M sodium hydroxide at 60 degrees C on viral infectivity was investigated. Inactivation of the following model and relevant viruses were followed as a function of time: human hepatitis A virus (HAV), canine parvovirus (CPV; a model for human parvovirus B-19) pseudorabies virus (PRV, a model for hepatitis B virus), and bovine viral diarrhoea virus (BVDV, a model for hepatitis C virus and human immunodeficiency virus). Infectivity of CPV was determined by a novel in situ EIA method which will prove useful for studies to validate parvovirus inactivation or removal. Infectivity of BVDV, PRV and CPV were shown to be reproducibly inactivated below the limit of detection by 0.1 M NaOH at 60 degrees C within 30 s. HAV was inactivated to below the limit of detection within 2 min. Treatment with heat alone also resulted in some log reduction for all viruses tested except for CPV which remained unaffected after heating at 60 degrees C for 16 min. Treatment of HAV with hydroxide alone (up to 1.0 m) at 15 degrees C did not lead to rapid inactivation. Collectively, these data suggest that 0.1 M NaOH at 60 degrees C for two min should be sufficient to inactivate viruses present in process residues.
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PMID:Inactivation kinetics of model and relevant blood-borne viruses by treatment with sodium hydroxide and heat. 1020 25

The hepatitis B and C viruses (HBV and HCV) and the human immunodeficiency virus (HIV) are the main causes of viral vasculitis in humans. The vascular lesions are classically ascribed to a variable combination of circulating immune complex deposition, cryoglobulinemia, and endothelial cell infection. Other viruses that can cause human vasculitis include the herpes viruses and parvovirus B19. The usual clinical manifestations of the viral infection are sometimes overshadowed by the vasculitis, which can be inaugural. With the exceptions of cytomegalovirus-and VZV-induced vasculitis, no specific treatments are available. A viral infection should be looked for routinely in patients with local or systemic vasculitis that does not admit of an obvious explanation.
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PMID:[Viral vasculitis not related to HBV, HCV and HIV]. 1021 17

Necrotizing vasculitis is a heterogeneous group of systemic diseases characterized by inflammation of blood vessel walls. There is current agreement that viral infections can play a central role in the pathophysiology of systemic vasculitides responsible for a broad spectrum of clinical patterns. The hepatitis B and C viruses (HBV and HCV), the parvovirus B19, the human immunodeficiency virus, the HTLV 1, and the cytomegalovirus are the viruses most often implicated. Only the HBV and HCV are associated with fairly well-defined clinical pictures. The conventional management of systemic vasculitis rests on administration of a corticosteroid with an immunosuppressive (usually cyclophosphamide). The decision to treat rests on the nature and severity of the vasculitis. In viral vasculitis, the goal of therapy is to treat both the systemic condition and its cause at the same time. In this situation, conventional immunosuppressive therapy promotes perpetuation of the viral infection, exposing the patient to chronic lesions and to relapses. Antiviral therapy has demonstrated clear evidence of efficacy in vasculitis related to the HBV and, to a lesser degree, the HCV. For the other viruses data, in the literature are scant.
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PMID:[Treatment of viral vasculitis]. 1021 19

Serum samples from two leopard cats (Felis bengalensis) and four Formosan gem-faced civets (Paguma larvata taivana) in Taiwan, September 1995, and nine leopard cats in Vietnam, August and December 1997, were examined for the prevalence of antibodies against feline parvovirus, feline herpesvirus type 1, feline calicivirus and feline immunodeficiency virus. All civets and nine of 11 leopard cats were shown to have antibodies against feline parvovirus (FPV), and FPV's were isolated from mononuclear cells in the peripheral blood of the six leopard cats.
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PMID:Serosurvey for selected virus infections of wild carnivores in Taiwan and Vietnam. 1047 95

While the importance of viral infections is well studied in domestic cats, only limited information is available on their occurence and prevalence in the European wildcat (Felis silvestris silvestris). The aim of this study was to determine the prevalence of antibodies to feline coronavirus (FCoV), calicivirus (FCV), herpesvirus (FHV), parvovirus (FPV), immunodeficiency virus (FIV), leukemia virus (FeLV), and FeLV antigenemia in 51 European wildcat sera. Samples were collected between 1996 and 1997 from wildcat populations in France, Switzerland, and Germany. Antibodies to FCoV were detected in two cats (4%) and FCoV RNA was detected in feces of one of these two cats. Antibodies to FCV, FHV and FPV were found at relatively low frequencies of 16%, 4%, and 2%, respectively. Antibodies to FIV were not detected. Although antigen and antibodies to FeLV were detected in 49%, and 75%, respectively, no evidence of FeLV-associated pathology was found. From the low prevalence of FCoV, FCV, FHV and FPV infections and from the fact that the European wildcats live solitarily, it was concluded that these viral infections do not spread readily within a population. Therefore, it may be assumed that release into the wild of European wildcats bred in captivity would not bring about a high risk of introducing of these viral infections to the free-ranging wildcats. As an exception, wildcats should be tested for absence of FIV infection before release if they were at risk to acquire this infection from domestic cats.
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PMID:Viral infections in free-living populations of the European wildcat. 1057 26

Genetic diagnosis is a revolutionary method that makes possible simultaneous viral isolation (detection) and identification. The method is so specific, sensitive, and rapid (non-culture) that leads not only to the diagnosis of viral infection, but also to prediction of the chemotherapy, monitoring during the therapy, and judging the efficacy of the treatment. Moreover, it contributes to understanding the disease pathophysiology. The qualitative results are sufficient for diagnosis, but quantitative analysis is sometimes necessary for the prediction of the efficacy and monitoring during treatment. It occasionally requires the numbers of genomic expression, the number of DNA/RNA copies, and the detection of point mutations for drug resistance. Many emerging and re-emerging infectious diseases, such as AIDS and viral hepatitis, are induced by viral infection via blood. The main causative agents of blood-borne viral infection are hepatitis B virus (HBV), hepatitis C virus (HCV), human immunodeficiency virus (HIV), human T cell leukemia virus type 1 (HTLV1), cytomegalovirus (CMV), Epstein-Barr virus (EBV), and human parvovirus B19. They play main roles in viral hospital infection. The risk of them being transmitted by transfusion of screened blood is very low, but it is always possible that infection may occur in a window period even after extensive blood screening tests. Therefore, to shorten a window period, genetic examinations will be accepted for screening tests in the near future. Prioritization of genetic examinations is needed to select the adequate method and sampling. After examinations, false positive and false negative results have to be extensively read out whether due to contamination or inhibition by agent such as heparin and hemoglobin. The causative virus should be decided by carefully eliminating passenger viruses or latent viruses. Because genetic examinations are so useful but occasionally yield false positive and negative results, genetic diagnosis should be judged totally by combination with other examinations, clinical signs, and clinical symptoms.
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PMID:[The role of genetic diagnosis in clinics--from the choice of ordering until reading the data]. 1059 Jun 77


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