<i>Plasmodium falciparum</i>Malaria and Perinatally Acquired Human Immunodeficiency Virus Type 1 Infection in Kinshasa, Zaire

Greenberg, Alan E.; Nsa, Wato; Ryder, Robert W.; Medi, Mvula; Nzeza, M; Kitadi, Nsimba; Matela, B.; Malanda, Nsuami; Davachi, Farzin; Hassig, Susan E.

doi:10.1056/nejm199107113250206

Cited by 104 publications

(58 citation statements)

References 18 publications

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“…Similarly, the survival of Western subjects with AIDS is prolonged by chemoprophylaxis of P. carinii pneumonia (52) and M. avium complex (236). However, in contrast, P. falciparum malaria was not found to affect the rate of disease progression in infants with congenital HIV-1 infection (134), and Mycoplasma infections (hypothesized as playing an important cofactor role [235]) were not found to contribute to the rate of disease progression (2).…”

Section: Impact Of Other Opportunistic Infectionsmentioning

confidence: 99%

Contribution of Immune Activation to the Pathogenesis and Transmission of Human Immunodeficiency Virus Type 1 Infection

Lawn

Butera²,

Folks³

2001

Clin Microbiol Rev

252

212

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The life cycle of human immunodeficiency virus type 1 (HIV-1) is intricately related to the activation state of the host cells supporting viral replication. Although cellular activation is essential to mount an effective host immune response to invading pathogens, paradoxically the marked systemic immune activation that accompanies HIV-1 infection in vivo may play an important role in sustaining phenomenal rates of HIV-1 replication in infected persons. Moreover, by inducing CD4+ cell loss by apoptosis, immune activation may further be central to the increased rate of CD4+ cell turnover and eventual development of CD4+ lymphocytopenia. In addition to HIV-1-induced immune activation, exogenous immune stimuli such as opportunistic infections may further impact the rate of HIV-1 replication systemically or at localized anatomical sites. Such stimuli may also lead to genotypic and phenotypic changes in the virus pool. Together, these various immunological effects on the biology of HIV-1 may potentially enhance disease progression in HIV-infected persons and may ultimately outweigh the beneficial aspects of antiviral immune responses. This may be particularly important for those living in developing countries, where there is little or no access to antiretroviral drugs and where frequent exposure to pathogenic organisms sustains a chronically heightened state of immune activation. Moreover, immune activation associated with sexually transmitted diseases, chorioamnionitis, and mastitis may have important local effects on HIV-1 replication that may increase the risk of sexual or mother-to-child transmission of HIV-1. The aim of this paper is to provide a broad review of the interrelationship between immune activation and the immunopathogenesis, transmission, progression, and treatment of HIV-1 infection in vivo

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Section: Impact Of Other Opportunistic Infectionsmentioning

confidence: 99%

Contribution of Immune Activation to the Pathogenesis and Transmission of Human Immunodeficiency Virus Type 1 Infection

Lawn

Butera²,

Folks³

2001

Clin Microbiol Rev

252

212

View full text Add to dashboard Cite

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“…[41,42] Other studies though have showed no major differences in malaria clinical outcomes between HIV positive and negative populations. [43][44][45] Many epidemiological, clinical and laboratory data has shown that women generally have higher serum immunoglobulin levels and mount stronger antibody responses following vaccination or infection compared to their male counterparts. [46] Our current study demonstrated then significant antibody levels between male and female participants.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of specific antibody responses to selected malaria vaccine candidates in Zimbabwean children

Marume

Nyandoro

Mutingwende

et al. 2015

Clinical Nursing Studies

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Introduction: There is high malaria related morbidity and mortality amongst infants and children in malaria endemic areas. An In-depth understanding of protective immunity correlates enables the long due necessary development of an effective malaria vaccine. This study aimed at evaluating antibody responses to apical membrane antigen 1 (AMA 1) that helps P falciparum entry into red blood cells, Glutamate rich protein (GLURP), an antigen expressed in the whole life cycle of the malaria causing pathogen, merozoite surface protein-1 (MSP 1) coding for a major antigen in the asexual stage of P falciparum and merozoite surface protein 3 (MSP 3), a polymorphic blood stage malaria antigen in Zimbabwean children living in malaria endemic areas. Methods: We characterized humoral immune responses to malaria vaccine candidates in a two year longitudinal survey among 136 children (6-16 years) from Burma and Kariba in Zimbabwe. Blood samples were collected and analyzed for malaria parasites, plasma and antibody titers against malaria vaccine candidates [MSP1, MSP3, GLURP, AMA] by ELISA technique. The blood samples were also checked for potential confounders like anemia, bilharzia and HIV sero-status using the ELISA technique. Results: Ig levels were significantly different (p < .0001) across the three time points, and against the different candidates (p < .0001). MSP3 had the highest (13,552.2) and GLURP the least (4,741.6) IgM titers. However, IgG, IgG1, IgG3 and IgG4 levels were highest against AMA compared to other vaccine candidates, 3) and anti-GLURP IgG4 (58.7)]. Anemia burden was about 44% at baseline with a threefold decrease (-16%) over the 12 month follow up. Conclusions: This study highlights the need for robust evaluation of several malaria vaccine candidates in combination to understand correlates of protective immunity as suggested by the significant antibody levels against the four vaccine candidates. Longer follow up periods are needed to assess the impact of continuous malaria exposure on host immune responses. Multivalent malaria vaccine development offer a better chance towards an efficacious malaria vaccine compared to monovalent vaccine. Antibody levels against the four vaccine candidates were significant suggesting that an ideal malaria vaccine should target more than one antigen.

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“…Among HIV-infected people, higher HIV load is associated with higher prevalence of Leishmania coinfection, and lower CD4 + cell count is associated with visceral and disseminated forms of leishmaniasis [94,95]. Visceral disease is more common among people with CD4 + cell counts of <300 cells/mm 3 , but disseminated infection usually does not occur until the cell count is <50 cells/mm 3 [97]. Visceral leishmaniasis is the fourth most common AIDS-related infection in southern Spain [97].…”

Section: Leishmaniasismentioning

confidence: 99%

“…Although parasitic CNS infection can occur in any host, some infections are more common among patients undergoing specific types of transplantation (table 1). The clinical and radiographic manifestations of parasitic CNS infection are often similar in immunocompromised and immunocompetent hosts, but certain infections may blunt or enhance these manifestations in immunosuppressed hosts [3,4]. Although neurologic symptoms vary somewhat by infecting parasite, they are mainly determined by the location(s) of the infection within the CNS (table 2).…”

mentioning

confidence: 99%

“…Although initial studies in areas where malaria and HIV infection are coendemic suggested no more than observed coexistence between these pathogens, subsequent studies detected not only an impact of HIV infection on the clinical course of malaria but also an impact of malaria on the clinical course of HIV infection [3,4,11,12]. For example, compared with people without HIV infection, HIV-infected people with malaria have a higher prevalence of fever, parasitemia, cerebral malaria, and severe or complicated malaria [5,[13][14][15][16][17][18].…”

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confidence: 99%

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Parasitic Central Nervous System Infections in Immunocompromised Hosts: Malaria, Microsporidiosis, Leishmaniasis, and African Trypanosomiasis

Snydman¹,

Walker²,

Kublin³

et al. 2006

Clinical Infectious Diseases

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Immunosuppression associated with HIV infection or following transplantation increases susceptibility to central nervous system (CNS) infections. Because of increasing international travel, parasites that were previously limited to tropical regions pose an increasing infectious threat to populations at risk for acquiring opportunistic infection, especially people with HIV infection or individuals who have received a solid organ or bone marrow transplant. Although long-term immunosuppression caused by medications such as prednisone likely also increases the risk for acquiring infection and for developing CNS manifestations, little published information is available to support this hypothesis. In an earlier article published in Clinical Infectious Diseases, we described the neurologic manifestations of some of the more common parasitic CNS infections. This review will discuss the presentation, diagnosis, and treatment of the following additional parasitic CNS infections: malaria, microsporidiosis, leishmaniasis, and African trypanosomiasis.As detailed in our previous article [1], the risk of acquiring fungal, viral, bacterial or parasitic infection is increased in patients receiving immunosuppressive therapy after transplantation and in people with advanced HIV infection. CNS infection occurs in 5%-10% of transplant recipients and up to 19% of patients with AIDS [2]. Patients with advanced HIV infection (CD4 + cell count, <200 cells/mm 3 ) and patients who require high levels of immunosuppression because of graft rejection or graft-versus-host disease are at greater risk than others of developing opportunistic CNS infections. Although parasitic CNS infection can occur in any host, some infections are more common among patients undergoing specific types of transplantation (table 1). The clinical and radiographic manifestations of parasitic CNS infection are often similar in immunocompromised and immunocompetent hosts, but certain infections may blunt or enhance these manifestations in immunosuppressed hosts [3,4]. Although neurologic symptoms vary somewhat by infecting parasite, they are mainly determined by the location(s) of the infection within the CNS (table 2).Evaluation of the immunosuppressed host presenting with neurologic symptoms or signs of infection should be guided by (1) the degree of immunosuppression, type of transplant received,

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Plasmodium falciparumMalaria and Perinatally Acquired Human Immunodeficiency Virus Type 1 Infection in Kinshasa, Zaire

Abstract: In this study malaria was not more frequent or more severe in children with progressive HIV-1 infection and malaria did not appear to accelerate the rate of progression of HIV-1 disease.

Cited by 104 publications

References 18 publications

Contribution of Immune Activation to the Pathogenesis and Transmission of Human Immunodeficiency Virus Type 1 Infection

Contribution of Immune Activation to the Pathogenesis and Transmission of Human Immunodeficiency Virus Type 1 Infection

Evaluation of specific antibody responses to selected malaria vaccine candidates in Zimbabwean children

Parasitic Central Nervous System Infections in Immunocompromised Hosts: Malaria, Microsporidiosis, Leishmaniasis, and African Trypanosomiasis

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