Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 58-year-old HIV-negative woman was admitted to our hospital with abdominal distension. She had a 5-year history of hypothyroidism and a 4-year history of diabetes mellitus. Physical examination revealed ascites. There was no lymphadenopathy or splenomegaly. Laboratory examination showed elevated levels of serum LDH and Al-p, polyclonal hypergammaglobulinemia, and was positive for anti-nuclear antibody, several autoantibodies and HCV-RNA. A computed tomographic scan of the abdomen and chest showed massive ascites, but there was no evidence of tumor masses or lymph node enlargement. Cytologic examination of the ascitic fluid revealed numerous abnormal lymphocytes which by flow cytometry demonstrated expression of CD5, CD19, CD20, and CD4. Cytogenetical analysis demonstrated a hyperdiploid karyotype, with numerical abnormalities. Southern blot analysis demonstrated rearranged monoclonal bands in JH and c-mycgenes. Polymerase chain reaction (PCR) analysis failed to detect the genomes of EBV and HHV-8 in the abnormal lymphocytes. A diagnosis of primary effusion lymphoma of B cell lineage was made. Following abdominal paracentesis, the patient remained in complete clinical remission for 7 months and died of an unrelated cause (cerebral bleeding). The present case demonstrated an HIV-, HHV-8-, and EBV-negative, and HCV-positive primary effusion lymphoma of B cell lineage, with a unique clinical course.
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PMID:[Human herpesvirus-8 negative primary effusion lymphoma with complete clinical remission after removal of ascites]. 1222 24

2 large epidemics of visceral leishmaniasis are presently occurring in Bihar State, India and in southern Sudan where it had not previously been a problem. Civil war which in turn led to sizable malnutrition and migration of many people and animals contributed greatly to the present epidemic. In southern Sudan, 30,000-40,000 people have already died. Villages have lost 30=65% of their population to visceral leishmaniasis, 4-40% carry the parasites, and 30-40% are immune to it. The epidemic is extending to the north. Other endemic areas in Africa include Kenya, many western and central African countries, and all the countries in northern Africa. Animal hosts include rats, genets, several cats, jackals, and dogs. The protozoan parasites Leishmania species are becoming more and more resistant to drugs which exacerbates these epidemics. The treatments include pentavalent antimonials, aminosidine, pentamidine, amphotericin B, liposomal amphotericin B, and sodium stibogluconate. The sandfly vector in India is beginning to exhibit resistance to DDT, but this is not yet a problem in Africa, however. The sandfly transmits promastigotes into the skin where an inflammatory factor in the sandfly saliva strengthens infectivity. They then infect phagocytic cells, especially macrophages, which essentially suppresses immunity. There they transform into amastigotes. Even though the body has very high levels of antileishmanial antibodies, the macrophages cannot eliminate the intracellular amastigotes. The parasites invade the spleen, liver, bone marrow, and lymph nodes--the macrophage-rich organs--which causes clinical symptoms. Some of these clinical symptoms include fever, wasting, splenomegaly, bone marrow failure, and lower than normal amounts of all cellular elements of blood. In HIV-positive Europeans who have lived in or visited endemic areas, visceral leishmaniasis has become an opportunistic infection. Their atypical features make it important to look for the parasites in tissues to diagnose it.
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PMID:Visceral leishmaniasis in Africa. 1231 71

Recently, the use of the ribonucleotide reductase (RR) inhibitor hydroxyurea (HU) in combination with nucleoside analogs has gained attention as a potential strategy for anti-HIV-1 therapy. However, appeal for the long-term use of HU in HIV-1 infection may be limited by its propensity to induce hematopoietic toxicity. We report a comparison of the efficacy and bone marrow toxicity of HU (400 and 200 mg/kg/day) with the novel RR inhibitors and free radical-scavenging compounds didox (DX; 3,4-dihydroxybenzohydroxamic acid; 350 mg/kg/day) and trimidox (TX; 3,4,5-trihydroxybenzamidoxime; 175 mg/kg/day) in the murine AIDS (LPBM5 MuLV) model of retrovirus infection. Infected mice received daily drug treatment for 8 weeks. Efficacy was determined by measuring drug effects on retroviral-induced disease progression (i.e. development of splenomegaly and hypergammaglobulinemia) and by evaluating splenic levels of proviral DNA. Bone marrow toxicity was evaluated by measuring peripheral blood indices (WBC, hematocrit and reticulocyte counts), femoral cellularity and by determining the numbers of hematopoietic progenitor cells (CFU-GM, BFU-E) per femur and spleen. Compared to infected controls receiving no drug treatment, disease progression was significantly suppressed by TX, DX and HU. However, HU was associated with mortality and induced significant hematopoietic toxicity in a time- and dose-dependent manner. Conversely, TX and DX effectively inhibited retrovirus-induced disease but did not induce hematopoietic toxicity. These results suggest that due to their reduced hematopoietic toxicity and ability to inhibit disease progression in murine AIDS, TX and DX may offer effective alternatives to HU therapy in HIV-1 infection.
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PMID:Suppression of retrovirus-induced immunodeficiency disease (murine AIDS) by trimidox and didox: novel ribonucleotide reductase inhibitors with less bone marrow toxicity than hydroxyurea. 1236 22

Achieving long-term pancellular expression of a transferred gene at therapeutic level in a given hematopoietic lineage remains an important goal of gene therapy. Advances have recently been made in the genetic correction of the hemoglobinopathies by means of lentiviral vectors and large locus control region (LCR) derivatives. However, panerythroid beta globin gene expression has not yet been achieved in beta thalassemic mice because of incomplete transduction of the hematopoietic stem cell compartment and position effect variegation of proviruses integrated at a single copy per genome. Here, we report the permanent, panerythroid correction of severe beta thalassemia in mice, resulting from a homozygous deletion of the beta major globin gene, by transplantation of syngeneic bone marrow transduced with an HIV-1-derived [beta globin gene/LCR] lentiviral vector also containing the Rev responsive element and the central polypurine tract/DNA flap. The viral titers produced were high enough to achieve transduction of virtually all of the hematopoietic stem cells in the graft with an average of three integrated proviral copies per genome in all transplanted mice; the transduction was sustained for >7 months in both primary and secondary transplants, at which time approximately 95% of the red blood cells in all mice contained human beta globin contributing to 32 +/- 4% of all beta-like globin chains. Hematological parameters approached complete phenotypic correction, as assessed by hemoglobin levels and reticulocyte and red blood cell counts. All circulating red blood cells became and remained normocytic and normochromic, and their density was normalized. Free alpha globin chains were completely cleared from red blood cell membranes, splenomegaly abated, and iron deposit was almost eliminated in liver sections. These findings indicate that virtually complete transduction of the hematopoietic stem cell compartment can be achieved by high-titer lentiviral vectors and that position effect variegation can be mitigated by multiple events of proviral integration to yield balanced, panerythroid expression. These results provide a solid foundation for the initiation of human clinical trials in beta thalassemia patients.
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PMID:Permanent and panerythroid correction of murine beta thalassemia by multiple lentiviral integration in hematopoietic stem cells. 1239 30

Tenofovir [9-(R)-2-(phosphonomethoxypropyl)adenine (PMPA)] and zidovudine [azidothymidine (AZT)] are potent anti-HIV agents that have shown a strong synergy in in vitro studies. In this paper we have investigated both the potentiality of this synergy in vivo and the possibility to administer AZT and PMPA simultaneously as a single drug AZTpPMPA. The pharmacokinetic studies reported here have shown that AZTpPMPA administered intraperitoneally in mice performs as a prodrug, providing a slow delivery of AZT and PMPA in circulation. C57BL/6 mice infected with the retroviral complex LP-BM5 were used to evaluate the efficacy of AZTpPMPA in inhibiting disease progression. Furthermore, the effectiveness of the heterodinucleotide was compared with that of AZT and PMPA, administered as single drugs, or as a combination (AZT plus PMPA). The results obtained showed that AZTpPMPA is able to reduce lymphoadenopathy (88%), splenomegaly (64%), lymph node BM5 proviral DNA content (49%) and hypergammaglobulinaemia (40%). However, upon AZT plus PMPA administration, similar (splenomegaly and lymphoadenopathy reduction) or better results (64% hypergammaglobulinaemia reduction and 75% lymph node BM5 proviral DNA content inhibition) were obtained. Furthermore, these results overlapped those obtained upon PMPA administration. Thus, no synergy between PMPA and AZT was observed in murine AIDS and administration of AZT does not improve the antiviral results obtained by PMPA administration.
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PMID:Inhibition of murine AIDS by a heterodinucleotide of azidothymidine and 9-(R)-2-(phosphonomethoxypropyl)adenine. 1240 19

In order to determine the main aetiologies associated with thrombocytopenia in a hospital setting of Cameroon, 180 adults with platelet counts <100x10(9)/L were examined and screened for a full blood count, thick and thin blood films, basic coagulation tests (activated partial thromboplastine time, a one-stage Quick's prothrombin time and a bleeding time), an HIV screening test as well as a bone marrow aspirate using standard methods. Other tests were selectively done as dictated by the suspected diagnosis. The major clinical findings among 180 cases included fever >37.5 C (53.9%), splenomegaly (45.6%) and haemorrhage (30.6%). The main laboratory findings were anaemia (defined as haemoglobin (Hb) <11g/dL) in 80.6% of cases and a positive thick blood film (all confirmed to be P. falciparum) in 30.6% of cases. Out of the 18 different aetiologies associated with a low platelet count in the group studied, malaria appears as the unique cause in 22.2% of cases. Petechial bleeding, bruising and epistaxis were the major forms of bleeding involved (69.1%, 27.3%, and 23.6% respectively). However, only 3 cases diagnosed with malaria showed any form of bleeding (mean malaria parasite densities >15,000/muL of blood in each case). No other haemostatic abnormalities were observed. It may be cost-effective for patients with low platelet counts in malarial regions to be systematically screened for malaria parasites.
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PMID:[Aetiologic factors and clinical features associated with thrombocytopenia in Cameroonese adults: the importance of Plasmodium falciparum malaria]. 1247 29

We report the case of a 25-year-old male Japanese homosexual with primary human immunodeficiency virus (HIV)-1 infection and early stage syphilis. Approximately 60 days after HIV exposure by sex with another man, the patient abruptly had high fever, after which he experienced a variety of severe, prolonged symptoms such as painful oral mucosa ulcerations, rash, lymphadenopathy, splenomegaly, and a 5.5-kg weight loss. Serum lactate dehydrogenase and liver biochemical test values were elevated. Antibodies to HIV by both enzyme-linked immunosorbent assay (ELISA) and Western blot (WB) test were negative at the time of symptom onset, but serum HIV-1 RNA level was 1 585 000 copies/ml. Antibody seroconversions were found on day 9 after the onset of symptoms by ELISA and on day 16 by WB test, suggesting primary HIV infection. Within 2 weeks of starting highly active antiretroviral therapy (HAART), all symptoms except lymphadenopathy were resolved, and the serum HIV-1 RNA level dramatically decreased to 5011 copies/ml, eventually becoming undetectable by the standard method. The patient has remained asymptomatic for the 18 months since symptom resolution after HAART, and HIV-1 RNA remains undetectable.
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PMID:A patient with primary human immunodeficiency virus infection for whom highly active antiretroviral therapy was successful. 1252

Case records of HIV infected patients were analyzed for identifying neurological manifestations. Eight patients (7 males) were identified to have probable HIV encephalopathy (in a period of 24 months) as per the CDC revised classification system. Their ages ranged from one year to ten years. The neurological manifestations noted included-developmental delay (2 cases), seizures (6 cases), acute onset alteration of sensorium (4 cases), aphasia (2 cases), loss of vision (2 cases), focal neurological deficits (6 cases), brisk deep tendon reflexes (7 cases), extensor plantar responses (5 cases) and signs of cerebellar dysfunction (2 cases). Other clinical features included growth failure, microcephaly, fever, lymphadenopathy, hepatomegaly, splenomegaly, pneumonia, otorrhea and oral candidiasis. Cerebrospinal fluid studies were normal. The neuroimaging features included cerebral atrophy and ventricular dilatation, cerebral infarction, basal ganglia calcification and cerebellar atrophy. Childhood HIV infection may have a variety of neurological abnormalities. HIV infection should be suspected in children presenting with unexplained neurological manifestations and growth failure.
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PMID:Neurological manifestations of HIV infection. 1265 56

Ninety-five HIV-infected children aged 3-5 and 6-14 years were examined. Clinical picture matched primary symptoms of stage IIV (phase of generalized lymphadenopathy by Pokrovsky V.I. classification, 1989) and included basic symptoms associated with HIV cytopathogenic action. Local opportunistic infections, either without damage of vital organs (phase IIIA of the secondary stage), or with damage of these organs (phase IIIB) were observed in patients with pre-AIDS. Generalized opportunistic infections and malignant tumors developed in patients with AIDS (phase IIIB and terminal stage IV). High frequency of bacterial infections, bacterial sepsis, splenomegaly, respiratory, gastrointestinal, cerebral, cardiac, common-infections syndromes, and rapid progression characterized the disease in young children. Local and generalized viral, fungal and protozoal infections were more frequently revealed in older children. Immunological alterations (T cell immunodeficiency, polyclonal activation of B lymphocytes, abnormalities of neutrophil metabolism) were diognosed in all children with phase IIV and were the most pronounced in young children. Progressive B lymphocyte polyclonal activation in young children, T cell immunodeficiency in older children and activation of neutrophil metabolism in those with pre-AIDS were observed. T cell immunodeficiency, B lymphocyte polyclonal activation, decreased neutrophil metabolism progressed steadily in all the patients with AIDS.
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PMID:Clinical and Immunological Features of HIV-Infection in Children Aged 3-5 and 6-14 Years. 1268 84

Thrombocytopenia is an important and common hematological abnormality in patients with HIV-1/HCV coinfection. Splenomegaly is a frequent finding in these patients and usually causes hypersplenism and thrombocytopenia. We analyzed the clinical results of a minimal invasive treatment (splenic artery embolization) for thrombocytopenia secondary to hypersplenism and refractory to other therapies in two hemophiliac patients, HIV seropositive and with cirrhosis due to chronic HCV infection. The results suggest that splenic artery embolization is a safe, relatively atraumatic and effective method for the treatment of splenomegaly and hypersplenism in selected patients with HIV-1/HCV coinfection.
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PMID:[Splenic artery embolization for the treatment of hypersplenism in hemophilic, HIV-1 and HCV seropositive patients]. 1287 7


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