Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

6 commercially available ELISA kits and 4 new Brazilian made methods for detecting HIV were compared on 2 panels of sera, 292 from AIDS patients, HIV-positives and negatives, and 180 sera from asymptomatic blood donors, including 90 HIV-positives. The kits tested were 5 ELISAs: Roche Diagnostica (Basel), Hoechst Enzygnostic (Sao Paulo), Virgo Electronuclionics (Columbia MD), Organon Teknika (Boxtel, Netherlands), Salck Industria e Comercio de Produtos Biologicos (Sao Paulo), and a passive hemagglutination test, (Salck Ind), and indirect immunofluorescence IIF (Virgo electronucleonics, Columbia), a dot blot (Embrabio, Empressa Brasiliera de Biotecnologia Ltda, Sao Paolo) and Karpas AIDS cell test, Fujichemical Industries Ltd (Chokeiji, Takaoka, Japan). The sensitivities ranged from 84.2% to 100% with no significant differences in sera from panel A. In panel B, the sensitivity of the PHA test was significantly lower than that of the ELISA and the AIDS cell tests. The specificities of the PHA and the AIDS cell tests were also lower than that of the ELISA. The costs of all the tests were similar, but the equipment needs varied. The simplest tests to perform were the dot blot assay, PHA and Karpas AIDS cell test. The Hoechst ELISA is simpler because it does not require dilution of the serum. The dot takes too long for use in a blood bank, 16-18 hours. Immunofluorescence tests would be practical in countries already screening blood for malaria or Changes disease. Brazil is not doing so on a large scale due to lack of political will. In countries with high incidence of malaria, Chagas disease, leishmania, hepatitis and leprosy, HIV test need to be tested on local sera because of possible B cell activation.
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PMID:Evaluation of enzyme-linked immunosorbent and alternative assays for detection of HIV antibodies using panels of Brazilian sera. 209 32

Epstein-Barr virus and HTLV-1 are both lymphotropic viruses, capable of immortalizing lymphocytes in vitro (Fig. 1). Both viruses have been sequenced and subjected to intense molecular biologic scrutiny, and in both cases genes believed to be important in lymphocyte immortalization have been identified. These viral genes are not homologues of cellular oncogenes, nor is there any evidence to suggest insertional mutagenesis. Rather, these genes alter the expression of a variety of cellular genes and, in so doing, alter the growth characteristics of the host cell. Infection with either virus is most likely to be asymptomatic, associated with a benign self-limited lymphoproliferation, or both, but in a small fraction of instances these benign lymphoproliferations give rise to a lymphoma or leukemia. In the case of the Epstein-Barr virus, a variety of cofactors have been identified that are important to the evolution of malignancy. These cofactors include immunosuppression in transplant recipients, cogenital immunodeficiency in the X-linked lymphoproliferative syndrome, human immunodeficiency virus infection in AIDS patients, and malaria in patients with endemic Burkitt's lymphoma. In the case of HTLV-1, cofactors have not been identified. Nonetheless, the importance of cofactors is suggested by the small fraction of the population infected by the virus who actually develop lymphoproliferative disease, and the long latency period between infection and the development of frank lymphoproliferative disease. In organ transplant recipients with lymphomas associated with Epstein-Barr virus infection, the EBV immortalizing/transforming genes are expressed in the malignant tissue. But in Burkitt's lymphoma and in adult T-cell leukemia/lymphoma, the EBV and HTLV-1 immortalizing/transforming genes are not detectably expressed. In Burkitt's lymphoma, it is suggested that the dysregulated myc gene renders the growth effects of Epstein-Barr virus latency genes superfluous. No comparable proto-oncogene translocation or activation has yet been identified in HTLV-1 lymphoma/leukemia.
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PMID:Human lymphotropic viruses associated with lymphoid malignancy: Epstein-Barr and HTLV-1. 217 3

Identifying the incubation period of HIV infection is important for individual prognoses, for developing and testing intervention strategies, for determining the reproductive rate of the disease, and for prevalence of the disease. Mathematical modeling of HIV infection in Africa is necessitated because the disease is more widespread and the immune system is constantly active due to the exposure to diseases such as malaria and tuberculosis. The Markov model for this analysis was selected because parametric estimation is not based on the time a stage is entered, but on the duration between observations and the stages at the time of observation. The HIV infected female prostitutes in the Pumwani area of Nairobi, Kenya (a population primarily of Tanzanian origin) have been identified as a study population since 1985, and seen every 6 months in clinic, or as needed. Data are constricted by the movement out of the area in the end stage of disease, which is only partially solved by tracking with community health workers. The stages identified in incubation estimation are stage 1: seropositive but symptom free (CDC stage II); stage 2: generalized lymphadenopathy (CDC stage III); stage 3: symptomatic disease (CDC stage IV); and stage 4: death. Data reflect the movement back and forth between stage 1 and 2, between 2 and 3, so the model is not a pure Longini model but rather a timed homogeneous staged model with reversible stages called transition parameters computed in a numerical differentiation. The Fortran computer program for the analyses is available from the authors. The results suggest a quick transition between seroconversion and lymphadenopathy (2.4 months) and unlikely reversal, with the mean waiting time until passage to stage 3 is approximately 2.6 years and conversions are common. Since opportunistic infections are treatable, this makes sense. Assuming a correct model, the estimation of the transition time of 20 months of h34 value of .01 and .05, the mean passage time from stage 1, 2, 3 to 4 (death) is 9.1, 8.9, and 6.2 years 12.9, 12.7, and 10.1 years respectively. The implications are that 1) when infectiousness is hypothesized to be not uniform, peak infectivity occurs earlier in Africa than in the West at least among prostitutes, or 2) if infectivity is constant throughout the incubation period, then HIV transmission must be higher in Africa to explain the high rate of infection.
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PMID:Transition dynamics of HIV disease in a cohort of African prostitutes: a Markov model approach. 217 19

Chloroquine is currently the drug of choice for treatment of acute attacks of Plasmodium falciparum malaria in chloroquine-sensitive areas. In areas of low level resistance, this drug may still be used (25 mg/kg of body weight in three days) in semi-immune patients. In case of failure, or in areas of high level resistance, quinine (25 mg/kg/day for 3 to 5 days) or, in spite of increasing resistance, Fansidar should be prescribed. Mefloquine, Fansimef and Halofantrine ought to be strictly prescribed to delay occurrence of resistance. Severe attacks require quinine by continuous intravenous infusion. Spleen enlargement does not usually require specific treatment unless poor tolerance is observed. Blood transfusions present a considerable risk of HIV transmission. Appropriate malaria treatment may avoid blood transfusions thus preventing HIV dissemination in Africa.
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PMID:[Treatment of Plasmodium falciparum malaria in Africa (except cerebral malaria)]. 219 75

This is a case report of a 24 year-old woman who is HIV-infected since three years (stage III B, CDC). She developed malaria tropica during her touristic stay in the Cameroons, Africa. No clinical complications were detectable even though she had a high parasitemia of 18% blood cells infected with Plasmodium falciparum. After quinine therapy defervescence occurred and blood smears were continuously free of malaria parasites. P. falciparum infection may increase HIV-related immunosuppression which favours the earlier occurrence of AIDS indicative opportunistic infections. Malaria in combination with HIV-infection can lead to a higher parasitemia; this does not necessarily lead to a higher rate of complications.
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PMID:[Malaria tropica in HIV infection]. 219 95

The acquired immune deficiency syndrome (AIDS) is fundamentally the same disease in all parts of the world, but the prevalence of microorganisms in an environment governs the patterns of disease arising from reactivated latent infections, invading pathogens and opportunistic infections. AIDS in Africa has certain characteristic presentations. Enteropathic AIDS is most common: Cryptosporidium and Isospora belli are identified in up to 60% of patients, but it is uncertain whether they are the causes of diarrhoea. Pneumocystis carinii pneumonia is rare. Tuberculosis, both pulmonary and extrapulmonary, is the supreme complicating infection. Herpes zoster is frequently the first clinical presentation, and has a 95% positive predictive value for HIV positivity. Measles may be more frequent in infants born to HIV-infected mothers, and appears to be worse in HIV-infected children. There is accelerated progress of both diseases in patients infected by HIV and Mycobacterium leprae. Salmonellosis is frequent. There is no direct interaction between malaria and HIV, but, by being a potent cause of anaemia, malaria enhances transmission of HIV to children through blood transfusion. HIV-positive subjects are liable to new or reactivated visceral leishmaniasis with dissemination to unusual sites. Cerebral toxoplasmosis is common. There are no apparent interactions between HIV and helminths, although there is one report of hyperinfection with Strongyloides stercoralis. Cryptococcal meningitis has high frequency. Infections with Histoplasma encapsulatum are common in tropical America, but there has been no increase of frequency of H. duboisii in Africa since the advent of AIDS.
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PMID:Opportunistic infections in AIDS in developed and developing countries. 220 Nov 7

There is concern that the impaired cell mediated immunity caused by the human immunodeficiency virus may increase the risk of severity of Plasmodium falciparum infection and could lead eventually to a decreased response to standard antimalarial treatment. In 1986, at Mama Yemo Hospital, Kinshasa, Zaire, the incidence of malaria was determined in a cohort of 59 patients who had recently acquired HIV-I infection through blood transfusion and in a cohort of 83 HIV-I seronegative controls who were recipients of HIV-I seronegative blood. All cohort patients were asked to visit the study physician whenever they developed fever. On each of these occasions thick film was examined for the presence of malarial parasites. HIV-I seropositive patients presented more often with episodes of fever per person month observation than HIV-I seronegative patients (P = 0.003). The total number of positive thick films per person months observation was significantly higher among HIV-I seropositive patients than among the HIV-I seronegative ones, but percentages of positive thick films per episode of fever were the same in both groups (46%). During a 5 month period, cohort patients presenting with a moderate attack of malaria were treated with oral quinine 20 mg/kg daily in two doses for 5 days. Twenty-three (92%) of 25 HIV-I seropositive patients and 28 (82%) of 34 HIV-I seronegative patients had a negative film 7 days after starting treatment. This study suggests that there seems to be no direct interaction of major clinical importance between HIV infection and malaria.
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PMID:Incidence of malaria and efficacy of oral quinine in patients recently infected with human immunodeficiency virus in Kinshasa, Zaire. 223 Jan 75

Africa is the continent most severely affected by the pandemic of immunodeficiency viruses (HIV-1 and HIV-2). Nowadays (1990), at least 3 million individuals are infected and about 300,000 cases of acquired immunodeficiency syndrome (AIDS) have been recorded. HIV infections started in the seventies as sporadic cases in remote areas and spread throughout black Africa where they are now epidemic, with high seroprevalence (1p. 100-20 p. 100), even in the general population. Due to heterosexual transmission, the groups at highest risk are female prostitutes and their customers and people with genital ulcers and/or sexually transmitted diseases (STDs). The vertical infection rates remain uncertain but may be estimated at 40 to 65 p. 100 of pregnancies in HIV-infected mothers. Blood transfusions are the third mode of infection because of high demands for blood (sometimes not tested) arising from severe anaemias in children (malaria and sickle cell anaemia), in pregnant women and in patients needing surgery. STDs causing ulcers undoubtedly are cofactors in the invasion by HIV, while the most important cofactors in AIDS progression are recurrent STDs, chronic activation of the immune system and repeated pregnancies that activate HIV-infected lymphocytes. The minimum mortality rate of AIDS is about 1 in 5000. Spatial, cultural and demographic factors should also be taken into consideration for all AIDS control programmes which must be integrated into the primary health care systems of African states.
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PMID:[Epidemiology of HIV infections in Africa]. 223 19

In sub-Saharian Africa, most HIV seropositive subjects carry either haematozoa (especially children) or antimalarial antibodies. Despite a transient decrease in cell-mediated immunity during malarial paroxysms, Plasmodium falciparum malaria does not seem to influence the course of the HIV infection. Paroxysms may be slightly more frequent or slightly more severe in HIV seropositive subjects, but they raise no diagnostic or therapeutic problem. Some cases of HIV contamination have been attributed to the blood transfusions required by malaria-induced anaemia. Prophylactic measures include early chemotherapy of malaria and detection of dangerous blood donors, if necessary by quick tests. Modern HIV tests avoid most of the false-positive reactions sometimes observed during malaria.
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PMID:[HIV infection and malaria]. 223 21

The high prevalence of hepatitis B markers in the Sudan (up to 80% of those surveyed) suggests the potential for a rapid spread of human immunodeficiency virus (HIV) since both viruses are transmitted in similar ways. Although clinical cases of acquired immunodeficiency syndrome (AIDS) have not been reported from Port Sudan, southern Sudan borders on several countries with a high prevalence of HIV infection. Sudan's National AIDS Committee plans a series of surveys to determine the prevalence of HIV infection in high risk groups and the general population in several geographic regions. The 1st such survey was conducted in Port Sudan in 1987 among 593 high-risk individuals (203 prostitutes, 103 lorry drivers, 118 prisoners, and 169 in mixed occupations). The study population included 330 males and 263 females. About half of the participants were married and in the 21-30-year age group. Over 75% had been exposed to hepatitis B and 76% had been treated for malaria, largely through injection. Overall, the incidence of non-sex-related risk factors for HIV infection among Port Sudan subjects was: injection, 48%; scarification, 40%; and tatoos, 38%. 32% reported a prior history of a sexually transmitted disease. 71% of the males had used prostitutes. Surprisingly, no study participants were positive for HIV infection. This finding presumably reflects Port Sudan's geographic isolation from other Central and East African countries with large numbers of HIV-positive individuals. On the other hand, Port Sudan is the site of importation of all goods by sea into the country and many people from other African and Arab countries are associated with the seaport. Thus, once the HIV virus is introduced by infected persons from other areas, the risk factors suggest the potential for rapid transmission.
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PMID:Serosurvey of prevalence of human immunodeficiency virus amongst high risk groups in Port Sudan, Sudan. 225 74


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