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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The author reports observations made during a visit with colleagues in Ethiopia. On the heels of the country's famine, she was surprised to see fertile land on an excursion 3 hours north of Addis Ababa. The harvest was expected to suffice for a 3-month period. While foreign technical and financial aid no doubt helped save countless lives during the famine, other serious health problems still remain in the country. In particular, the writer notes the ongoing high rates of maternal and infant mortality (IMR). The national IMR of 168/1000 live births is heavily fueled by diarrheal illness, infectious disease, and malaria. Nationally, only 15% of 2 year olds have completed an immunization program. Women have a 1:30 chance of dying in pregnancy or during childbirth, with over 1/2 due to illegal abortions and other maternal health problems. While family planning may be available, cultural norms limit the number of subscribers. Leprosy remains a significant problem, and AIDS was gaining notice in 1989. Moreover, drug supply constraints and the paucity of national medical doctors help stymie any efforts toward positive change. The writer encourages continued foreign aid.
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PMID:Ethiopia between famines. 238 25

Long-term cultures were established of HTLV-III-infected T4 cells from patients with the acquired immune deficiency syndrome (AIDS) and of T4 cells from normal donors after infection of the cells in vitro. By initially reducing the number of cells per milliliter of culture medium it was possible to grow the infected cells for 50 to 60 days. As with uninfected T cells, immunologic activation of the HTLV-III-infected cells with phytohemagglutinin led to patterns of gene expression typical of T-cell differentiation, such as production of interleukin-2 and expression of interleukin-2 receptors, but in the infected cells immunologic activation also led to expression of HTLV-III, which was followed by cell death. The results revealed a cytopathogenic mechanism that may account for T4 cell depletion in AIDS patients and suggest how repeated antigenic stimulation by infectious agents, such as malaria in Africa, or by allogeneic blood or semen, may be important determinants of the latency period in AIDS.
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PMID:Long-term cultures of HTLV-III--infected T cells: a model of cytopathology of T-cell depletion in AIDS. 241 2

This review describes the transmission, clinical picture and immunological abnormalities of HIV infection in children in general, and the special problems of AIDS in African children. The review begins with a thorough introduction to the epidemiology of AIDS. Transmission to children generally involves vertical transmission by placental transfer or transmission of HIV via transfusion of blood and blood products, or by contaminated needles. Casual transfer is unknown, and only a few cases of transmission via breast milk are known. The clinical picture of HIV infection in infants and children differs from that in adults in 3 important aspects: earlier onset, different clinical presentation and existence of AIDS embryopathy. The average onset was 5 months of age. The most common symptoms in young children are chronic interstitial pneumonitis without demonstrable etiology, hepatomegaly, failure to thrive, adenopathy, diarrhea, oral or perineal thrush, eczema and thrombocytopenia. The common opportunistic infections are pneumocystis carinii pneumonia, cytomegalovirus, Epstein-Barr virus, Cryptosporidium diarrhea, pyogenic infections of the middle ear and gram-negative septicemia. Several infections seen in adult AIDS cases are rare in children: mycobacterium avium-intracellulare, toxoplasma gondii, hepatitis B, as well as Kaposi's sarcoma, malignant lymphoma and cardiac abnormalities. The AIDS embryopathy or HIV dysmorphic syndrome is characterized by immunological abnormalities, growth failure, and craniofacial dysmorphism, particularly microcephaly, prominent box-like forehead, hypertelorism, flattened nasal bridge, obliquity of the eyes, blue sclerae and patulous lips. AIDS in African children is extremely difficult to diagnose because of similarities between the presenting symptoms and those commonly seen in sick children there, many of whom are also immune compromised. Where serotesting is available, the picture is complicated by cross reaction between the test agents and some factor found in sera from malaria patients. Seropositivity in some areas is high, increased by the prevalence of transfusion and injection treatments. Diagnosis is made more difficult by lack of laboratory facilities and difficulties in follow-up for pediatric patients. The CDC definitions of AIDS and ARC, and the WHO/CDC definitions of AIDS are appended.
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PMID:Human immunodeficiency virus infection in childhood. 245 15

From the moment WHO was established in 1948, the control of venereal diseases was felt to deserve highest priority, together with activities to control malaria and tuberculosis. International action was needed in view of the high morbidity and mortality from venereal diseases, their serious human and social consequences, and the prevalence of congenital syphilis and other sexually transmitted diseases (gonorrhoea, chancroid, venereal lymphogranulomatosis, granuloma inguinale). WHO immediately set up a global programme for the control of STDs and, with the participation of other agencies, especially UNICEF, furnished countries with assistance in the form of personnel, equipment and funds for the operation of programmes to assess the extent and impact of STDs and to plan and implement practical measure of control. The 1950s witnessed a steady and considerable decline in syphilis and gonorrhoea and many health authorities relaxed their control activities and efforts to maintain public awareness of the problem. In contrast to the prevailing optimism, WHO repeatedly stressed the possibility of a renewed upsurge of STDs. In the 1960s and 1970s, there was a sharp rise in STDs, both in the "classic" diseases (the five venereal diseases mentioned above) and also in the "second generation" STDs (chlamydial infection, genital herpes, human papillomavirus and other infections). Through its programme for the control of STDs, WHO put forward suitably designed control strategies, essentially based on information and education for health, screening for STDs, diagnosis and treatment of cases, contact tracing, and the training of health personnel. By the end of the 1970s, the bacterial, but not the viral STDs, had been contained in the industrialized countries. In many of the developing countries, STDs remained a priority public health problem, above all on account of the seriousness of their sequelae. In 1981, a new sexually transmitted disease-the acquired immunodeficiency syndrome (AIDS)-was identified. As of 1982, the WHO Programme on STDs organized meetings to define the extent of the problem, compare experience, promote and coordinate research and propose strategies for prevention. In 1987, WHO established a Global Programme on AIDS. It is clear that the control of STDs is now more than ever a priority. We have strategies for the prevention and control of STDs and the WHO Programme will continue to collaborate closely with countries in strengthening their national control programmes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The campaign against sexually transmissible diseases and endemic treponematoses]. 245 57

T lymphocytes, in contrast to antibodies, appear to recognize primarily a limited number of antigenic sites on any given antigenic protein. We find that a single site can so dominate the T-cell repertoire that the presence or absence of a response to one immunodominant site can make the difference between a high responder and a low responder, even though low responders respond to other sites almost as well as high responders. Besides interaction with major histocompatibility complex (MHC) molecules, the mode by which the antigen is processed into fragments for T-cell recognition also determines which sites are seen. The products of natural processing of the protein appear to be larger than the synthetic peptides and contain structures which hinder binding to certain MHC molecules or to the T-cell receptor. A third factor in immunodominance is the intrinsic structure of the antigenic site. We have shown that amphipathic helices have a higher than random chance of being immunodominant, and have developed a computer program to locate such structures in protein amino acid sequences. We prospectively predicted sites in the malaria circumsporozoite protein and found that the four most widely recognized sites in an endemic area of West Africa were all predicted. Similarly, we identified two helper T-cell sites from the HIV (AIDS virus) envelope, and have now shown that immunization with these elicits enhanced antibody responses to the whole envelope when injected into monkeys. These sites are also recognized by human T cells from volunteers who had been immunized with a recombinant vaccinia virus expressing the HIV envelope. Also, because cytotoxic T lymphocytes (CTLS) may play a critical role in defence against AIDS, we have used a recombinant vaccinia virus and transfectants expressing the HIV envelope gene to induce specific CTLS against the HIV envelope. Using synthetic peptides, we were able to identify the first CTL recognition site in the AIDS virus. These results may contribute to the rational design of vaccines.
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PMID:Structural features of T-cell recognition: applications to vaccine design. 247 71

Immunodominant T-cell antigenic sites can so dominate a response that their presence leads to high responsiveness and their absence to low responsiveness. Therefore, it is important to locate such sites for vaccine development. Factors that lead to immunodominance include features extrinsic to the structure of the site itself, such as the major histocompatibility complex (MHC) molecules of the host and the types of fragments produced by processing of the protein antigen before the T cell sees it. They also include factors intrinsic to the structure of the T-cell site, that determine a repertoire of potential immunodominant sites from which the extrinsic factors select a subset that will be immunodominant in a given individual. We have focused on one of these intrinsic factors, helical amphipathicity, that we have found to be a common feature among both helper and cytotoxic T-cell antigenic sites, suggesting that the same physical principles apply to sites seen in association with class I and class II MHC molecules. We have used this feature to locate immunodominant epitopes on the circumsporozoite protein of the Plasmodium falciparum malaria parasite and the envelope protein of the AIDS virus. Both helper and cytotoxic T-cell epitopes were identified. At least in the case of the helper T-cell sites, it was striking that the same sites in both the malaria and AIDS proteins studied that were immunodominant in the mouse were also immunodominant in the human, an indication that the same principles apply across species, and that the animal model will be useful for identifying sites to be used in vaccines for humans. These sites have been coupled with neutralizing antibody sites to produce artificial constructs that can elicit antibodies. It is hoped that the rational design of more complex versions of these artificial constructs will produce vaccines that are more effective than the natural pathogen proteins used in subunit vaccines, since such pathogen protein antigens have been selected through evolution to evade the immune system, not to optimize immunogenicity.
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PMID:Mechanisms of immunodominance in T-cell recognition, with applications to vaccine design. 247 31

About 120,000 infants are born each year with sickle cell disease (SCD) in Africa. The majority have Hb SS, but Hb SC and Hb S/beta+ thalassaemia are common in west Africa. The development of Plasmodium falciparum and P. malariae is partially inhibited in the Hb SS red cells, but malaria precipitates both haemolytic and infarctive crises, and is the commonest and most important cause of morbidity and mortality. The pneumococcus is likely to be the second major infectious cause of sickness and death. In one rural community, there were less than 2% of the expected number of subjects with SCD surviving beyond 5 years of age. Genetic factors improving prognosis include (1) the Senegal beta chain haplotype, which is linked to a high level of Hb F, and (2) alpha+ thalassaemia. Of environmental factors improving prognosis, the family is of first importance. The commonest age of presentation is 1-3 years. Children present with anaemic crises (malaria, splenic sequestration, folate deficiency, and possibly aplastic), infarctive crises (hand-foot syndrome, bone-pain, pulmonary and abdominal) or acute infections (malaria, pneumonia, septicaemia, meningitis, osteomyelitis). Tragically, many patients in central Africa have been infected by the human immunodeficiency virus (HIV) through blood transfusions; they present with generalised lymphadenopathy and other features of the acquired immunodeficiency syndrome (AIDS). The principles of management are (1) to ensure freedom from malaria, (2) to continue folic acid supplements, (3) to give blood transfusions only when anaemia endangers life, (4) to control pain, (5) to restore hydration, and (6) to prescribe broad spectrum antibiotics in large dosage and without delay, but only when there are definite indications, such as fever (greater than 39 degrees C), acute pulmonary disease, meningitis, and acute osteomyelitis. The advent of HIV and AIDS makes the control of SCD of even greater importance. Principles of control are (1) early diagnosis through appropriate laboratory techniques and selective screening, (2) education of parents, patients, health professionals and public, and (3) the maintenance of health at sickle cell clinics; measures must include antimalarial prophylaxis. SCD programmes should be integrated with primary health care and AIDS control programmes.
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PMID:The presentation, management and prevention of crisis in sickle cell disease in Africa. 265 Jul 73

We conducted a cross-sectional study to determine the serological response to malaria in an HIV-1 infected population and in a control population in a region of high malaria transmission. The study group consisted of 66 hospitalized patients with clinical acquired immunodeficiency syndrome (AIDS) and 70 trauma patients without clinical AIDS (controls). Mean optical densities of antibody produced against RESA-4, RESA-8, RESA-11, (PNAN)5 and (NAAG)5 synthetic peptides of Plasmodium falciparum were compared between HIV-1 seropositive and HIV-1 seronegative patients using non-parametric statistics. HIV-1 seropositive patients with clinical AIDS had significantly less antibody to the synthetic P. falciparum ring stage peptide, RESA-8 (P = 0.001), than a comparable group of seronegative patients. Antibody levels were also low for the other ring stage peptides, RESA-4 (P = 0.024) and RESA-11 (P = 0.024). Although not statistically significant, antibody levels among the HIV-1 seropositive trauma patients were higher than among the HIV-1 seronegative trauma patients. During HIV-1 infection, a polyclonal B cell activation may occur as noted in the HIV-1 seropositive trauma patients, but with increased immunosuppression in advanced clinical AIDS, B cell stimulation appears to be diminished. This results in decreased production of malaria antibody.
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PMID:Immunological effects of HIV-1 infection on the humoral response to malaria in an African population. 268 20

The aetiology of severe anaemia (haemoglobin less than 7.0 g dl-1) has been studied in 37 pregnant Zambians. Aetiology was usually multiple; 31 (84%) had Plasmodium falciparum malaria, 23 (62%) were folate deficient, 13 (35%) were iron deficient, one had sickle-cell anaemia and one had the acquired immunodeficiency syndrome (AIDS). Folate deficiency was most often secondary to malarial haemolysis: iron deficiency was nutritional, but hookworm was contributory in about one-third of patients. The anaemia of malaria and folate deficiency was both more common and more severe than anaemia due to iron deficiency; it was seen in younger women although primigravidae were not over-represented, it occurred earlier in pregnancy, and was associated with low birthweight. AIDS must now be included in the differential diagnosis of anaemia in pregnancy. Vigorous antimalarial treatment and prophylaxis are essential in the management and prevention of anaemia in pregnancy. Total dose iron infusion is indicated only when severe iron deficiency anaemia has been proven, and must be accompanied by antimalarial therapy and folic acid supplements. Because of the risk of transmission of human immunodeficiency virus, it is more important than ever to prevent anaemia and malaria in pregnancy, and to give blood transfusion only as a life-saving treatment.
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PMID:The aetiology of severe anaemia in pregnancy in Ndola, Zambia. 268 77

One of the most intriguing aspects concerning the pathogenesis of AIDS is the long period of latency of the HIV in human cells, not causing any cytopatic effect in some and, on the other hand, causing cell destruction, at short periods, in others. The various agents and the mechanisms they adopt to reactivate the latente HIV, were described. Also the frequent epidemiological observation on the presence of both such agents and the HIV in AIDS patients allowed the authors to speculate on the probable important role of a cohort of co-factors which determine the destiny of such individuals. Special considerations were made in respect to the hepatitis B virus, cytomegalovirus, herpesviruses (HHV-1, e and 6), EB virus, HTLV-1 and 2 retroviruses, group B arbovirus Maguary, malaria and other endemic infectious diseases which victimize millions of Brazilians. Accepting the importance of such co-factors acting on the viral gens that regulate the HIV expression in the host cell, it was speculated on the possible role of vaccines, such as the hepatitis B vaccine, and some antiviral drugs which could be useful in the indirect prevention of AIDS-disease in both HIV-carriers and those practising AIDS-high-risk-activities.
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PMID:[Pathogenesis of AIDS: possible role of co-factors in HIV reactivation]. 269 96


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