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)

Mouse hepatitis virus type 3 (MHV3) appears to be an excellent model for the study of the relationship between viral-induced immunodeficiency and the development of chronic disease. Animal surviving acute hepatitis develop a chronic disease characterized by viral persistency in various organs, by a humoral immunodeficiency, and eventually die within the next three months postinfection. To verify if B cell immunodeficiency occurs during the chronic disease, percentage and absolute number of bone marrow B lineage cell subpopulations were recorded at various times postinfection (p.i.) in pathogenic L2-MHV3-infected (C57BL/6 x A/J) F1 mice. Absolute numbers of B (cmu+smu+) cells decreased as early as three days p.i. up to 15 days p.i., and then gradually returned toward normal values in L2-MHV3-infected mice during the chronic disease. In contrast, pre-B (cmu+smu-) cells were less significantly decrease during the chronic disease. In addition, abnormally enlarged cells (> 13 microns) were detected either in bone marrow pre-B or B cells from L2-MHV3-infected mice.
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PMID:Impairment of bone marrow pre-B and B cells in MHV3 chronically-infected mice. 883 Apr 80

Such nonpercutaneous routes of hepatitis C virus (HCV) transmission as sexual and perinatal spread are relatively inefficient. Several observations have been cited to support a role for sexual transmission of hepatitis C. Approximately 10% of persons with reported cases of acute hepatitis C in the United States report a history of potential sexual exposure. Anecdotal cases of sexual transmission have been reported, and HCV nucleotide sequence homology has been observed in viral isolates from sexual partners. Similarly, the prevalence of HCV infection is increased in groups with a high risk of exposure to sexually transmitted viral infections. Other observations, however, weigh against sexual transmission of HCV infection. Sexual transmission is negligible in sex-partner studies; alternative risk factors account for many cases of apparent sexual transmission between sexual partners; the prevalence of HCV infection in high-risk groups is much lower than that of other sexually transmitted infections; and the risk of apparently sexually transmitted HCV infection does not always correlate with intensity and duration of sexual exposure. The United States Public Health Service has estimated that the risk of sexual transmission is approximately 5%, well below the risk of sexual transmission of hepatitis B or human immunodeficiency virus (HIV). Similarly, perinatal HCV infection, though documented to occur, is unusual, except in babies born to mothers with very high levels of HCV RNA, including mothers with concomitant HIV infection. Weighing many, often conflicting reports, the United States Public Health Service has estimated that the likelihood of perinatal infection is low, on the order of 5% to 6%, and that breast feeding does not increase the risk of HCV infection in infants of mothers with hepatitis C. Current data do not support household exposure as a risk for HCV infection.
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PMID:Sexual and perinatal transmission of hepatitis C. 930 67

Patients with aids are at increased risk of opportunistic and non opportunistic infections. It is now known that the incidence can be reduced by prophylactic measures and/or the use of vaccines. HIV infection produces an elevated frequency of severe pneumococcal disease with a rate of bacteriemia caused by Streptococcus pneumoniae 150-300 fold greater than rates reported in non-HIV infected people. For this reason, pneumococcal vaccine should be administered as early as possible in the course of the infection. Besides, the antibody response may be significantly higher for asymptomatic persons. Acute hepatitis caused by hepatitis B virus is milder than in non HIV infected patients but chronic disease is more frequent. The prognosis is worse and there is higher risk for infecting another persons. Hepatitis B vaccine is indicated for all the patients with HIV and negative serology for hepatitis B virus. Influenza vaccine is of limited effectiveness due to the high variability of the virus. Besides, influenza incidence is low among approximately young adults, HIV related immunodeficiency increased influenza risk only minimally, the vaccine is administered yearly and HIV-replication can increase in temporal association with vaccination. For all these reasons, fewer hospitalizations and deaths are prevented making it a far less cost-effective prevention strategy than pneumococcal vaccination. The risk of Haemophilus influenzae infections is elevated, but the vaccine is not routinely recommended because the more frequent serotype in HIV infected patients is b. For these subjects, passive immunization with immunoglobulin may also be necessary to provide protection. In conclusion, pneumococcal and hepatitis B vaccination is a reasonable prevention strategy for HIV infected patients at all stages of immunodeficiency. Influenza and H. influenzae vaccination are not recommended and alternative prevention strategies may be done.
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PMID:[Which are the vaccines that human immunodeficiency virus infected patients must receive?]. 978 Apr 28

We report a case of simultaneous infection with hepatitis B virus (HBV) and human immunodeficiency virus type 1 (HIV-1) in a 26-year-old Japanese homosexual man. He was admitted to our hospital for acute hepatitis caused by HBV. At that time, HIV-1antibody (Ab) was not detected in his serum. After 6 months, he was readmitted to our hospital for further examination of his liver because of confined liver enzyme abnormalities. Anti-HIV- Ab was detected in his serum by both enzyme immunosorbent assay (EIA) and particle agglutination (PA). His serum HIV-1 RNA level was 50 x 10(4) copies/ml and serum levels of HBV DNA polymerase (DNA-P) and HBV DNA were 6535cpm and 3 plus (>1000 copies/ml). His clinical course and laboratory data suggested progression from acute to chronic hepatitis related to coinfection with HIV-1. The diagnosis was chronic active hepatitis caused by HBV as an opportunistic infection due to coinfection with HIV-1. We began highly active antiretroviral therapy (HAART) because interferon (IFN) therapy was ineffective. HAART was started at an initial dosage of 600 mg zidovudine (AZT), 300 mg lamivudine (3TC), and 2400 mg indinavir (IDV) daily. After 4 weeks, the serum level of HBV DNA-polymerase (p) had decreased markedly to 37cpm and that of HIV-1 RNA had decreased to below the sensitivity threshold, indicating considerable suppression of the replication of these viruses by the treatment. But HBV DNA remained at low levels. Although the incidence of HBV infection in patients with HIV-1 infection has been reported to be high in the United States and Europe, simultaneous HBV and HIV-1 infection leading to persistent HBV infection is rare.
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PMID:Highly active antiretroviral therapy used to treat concurrent hepatitis B and human immunodeficiency virus infections. 1021 32

In Romania and other countries, therapeutic injections have been associated with transmission of hepatitis B and C viruses, human immunodeficiency virus type 1 (HIV-1), and other bloodborne pathogens. During 1997-1998, acute hepatitis B was associated with recent injections in Romanian children aged <5 years. Injection-associated bloodborne pathogen transmission occurs when infection-control practices are inadequate, and overuse of injections to administer medications might increase opportunities for transmission. To estimate the frequency of therapeutic injections and to describe the attitudes and practices of adults about injections to administer medications, local health departments in Romania surveyed the general population of four districts (Hunedoara, Iasi, Mures, and Prahova [1997 combined population: 2.8 million]) in June 1998. This report summarizes results from these surveys, which indicate that injections are used frequently to administer medications in Romania.
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PMID:Frequency of vaccine-related and therapeutic injections--Romania, 1998. 1022 2

It is now widely accepted that 85% or more of individuals with acute hepatitis C virus (HCV) infection progress to chronic hepatitis, and chronic hepatitis C is a known risk factor for cirrhosis and hepatocellular carcinoma (HCC). However, there has been much controversy about the inevitability of developing cirrhosis and HCC and the time frames in which they are likely to occur. Natural history studies have provided varying estimates of the risk of progression in chronic hepatitis C. Part of this variation may be a result of viral-specific, host, and/or environmental factors, but much of it undoubtedly is a result of the difficulties of doing natural history studies in this disease: acute onset is rarely identified, chronic infection is often asymptomatic, and the duration of disease is prolonged. Three types of studies--prospective, retrospective, and retrospective-prospective (nonconcurrent prospective)--have attempted to determine the clinical outcomes of chronic HCV infection and have provided widely varying estimates. The combined population data indicate that the disease progresses slowly over approximately 30 years, on average. Approximately 20% of infected individuals will progress to fibrosis and cirrhosis. Of these, approximately 20% will progress to HCC. The likelihood of progression appears to be independent of genotype or viral load but increases with alcohol intake, male sex, age over 40 years at infection, and coinfection with human immunodeficiency virus (HIV) or hepatitis B virus (HBV). Results of ongoing nonconcurrent studies are needed to determine disease progression in the third, fourth, and fifth decades of infection and to better define the factors that affect progression.
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PMID:Natural history of hepatitis C. 1065 49

There are increasing molecular and clinical evidences that the effects of human immunodeficiency virus (HIV) infection can be modified by coinfection with other viruses. The objective was to investigate the viral interaction between HIV and hepatitis C virus (HCV) after HCV superinfection. A 16 year-old pregnant woman was evaluated because of icteric acute hepatitis. Admission laboratory tests showed the following results: ALT 877 IU/L; AST 1822 IU/L; bilirubin 6.79 mg/dl. Diagnosis of acute HCV was based on detection of serum HCV RNA by PCR and anti-HCV seroconversion. ELISA for anti HIV testing was positive and confirmed by western blot. Serum markers for other viruses were negative. The patient was followed during 19 months; serum samples were taken monthly during this period for detection of plasma HIV and HCV RNA. Levels of plasma HIV-RNA were positive in all samples tested before and after the onset of acute hepatitis C. Six months later and a for two month period, and 13 months later for a period of one month HIV viremia was undetectable; then HIV-RNA in plasma was detectable again. In conclusion, HCV superinfection may have temporarily interfered with HIV replication in our patient. The following observations support our hypothesis: it has been demonstrated that HIV-1 replication is suppressed by HCV core protein which has transcriptional regulation properties of several viral and cellular promoters. Clinical implications of this event are not generally known and the interaction between these two viruses in dual infections is worth considering.
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PMID:In vivo down regulation of HIV replication after hepatitis C superinfection. 1075 1

We report the case of two patients in whom acute hepatitis A was associated with a marked and prolonged increase in human immunodeficiency virus type 1 (HIV-1) viral load. Although in one patient the rise in HIV-1 RNA might also have been related to the interruption of antiretroviral therapy, we also observed a similar pattern in the other patient who had a stable undetectable plasma viraemia prior to acute hepatitis and never received treatment with anti-retrovirals. Our observation supports the hypothesis that immune activation that is induced by acute hepatitis A virus (HAV) infection may trigger HIV-1 replication. This highlights the importance of maintaining antiretroviral therapy throughout the acute phase of hepatitis A and of preventing HAV infection through active immunization.
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PMID:Persisting HIV-1 replication triggered by acute hepatitis A virus infection. 1084 87

Acute hepatitis led to abnormal coagulopathy, bleeding, and death in a nonhemophiliac infant infected with the human immunodeficiency virus, possibly due to zidovudine or ritonavir or both. Acute hepatitis during ritonavir treatment and episodes of spontaneous bleeding have been reported in patients with hemophilia. Zidovudine is associated with elevated liver enzymes, elevated bilirubin, and hepatomegaly leading to abnormal coagulopathy, bleeding, and death in adults. A temporal relationship between the start of combination antiretroviral therapy and onset of hepatosplenomegaly and rise in liver enzymes suggests that zidovudine or ritonavir, or both, are the likely cause of this adverse event. Ritonavir is believed to cause direct hepatotoxicity, probably by inducing acute mitochondrial toxicity, and may hasten reverse transcriptase inhibitor-induced liver toxicity. Liver function of patients receiving a combination of nucleoside reverse transcriptase inhibitor and protease inhibitors should be closely monitored.
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PMID:Acute hepatitis and bleeding possibly induced by zidovudine and ritonavir in an infant with HIV infection. 1099 9

We conducted a descriptive study in 9 cases of acute hepatitis A diagnosed in patients with human immunodeficiency virus (HIV). Despite the small number of cases studied, the results indicate that moderate HIV infection does not impair the natural history of acute hepatitis A.
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PMID:Occurrence of acute hepatitis A in patients infected with human immunodeficiency virus. 1158 8


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