Progressive Multifocal Leukoencephalopathy and JC Virus Genotypes in West African Patients With Acquired Immunodeficiency Syndrome

1999 ◽  
Vol 123 (5) ◽  
pp. 395-403
Author(s):  
Sylvester C. Chima ◽  
Hansjürgen T. Agostini ◽  
Caroline F. Ryschkewitsch ◽  
Sebastian B. Lucas ◽  
Gerald L. Stoner
Keyword(s):  
Progressive Multifocal Leukoencephalopathy ◽  
Acquired Immunodeficiency Syndrome ◽  
Jc Virus ◽  
West African ◽  
Sub Saharan Africa ◽  
Virus Genotypes ◽  
Acquired Immunodeficiency ◽  
Sub Saharan ◽  
African Patients ◽  
Immunodeficiency Syndrome

Abstract Objective—Progressive multifocal leukoencephalopathy is caused by polyomavirus JC in immunosuppressed patients. JC virus genotypes are identified by sequence analysis of the viral genome. Despite the prevalence of acquired immunodeficiency syndrome in sub-Saharan Africa, few cases of progressive multifocal leukoencephalopathy have been reported from this region. Here we describe 4 African cases and provide an analysis of viral genotypes. Methods.—Immunohistochemical staining by labeled streptavidin-biotin for capsid protein antigen was performed on all cases. Polymerase chain reaction amplification of viral genomic DNA was followed by direct cycle sequencing. Results.—JC virus type 3 was identified in 2 cases, and type 6 was isolated in 1 case. The viral regulatory region from 1 case showed an uncommon rearrangement pattern. Conclusions.—Progressive multifocal leukoencephalopathy in West African patients with acquired immunodeficiency syndrome is caused by African genotypes of JC virus (types 3 and 6). The prevalence of disease in this autopsy series from sub-Saharan Africa (1.5%) was less than has been reported from Europe and the United States (4% to 10%) and may be partly due to biological differences in JC virus genotypes. Further studies will be needed to confirm this observation.

scholarly journals Prevalence of Pneumocystosis in Sub-Saharan Africa and Helminth Immune Modulation

2021 ◽  
Vol 8 (1) ◽  
pp. 45
Author(s):  
Luis Fonte ◽  
María Ginori ◽  
Enrique J. Calderón ◽  
Yaxsier de Armas
Keyword(s):  
Immune Responses ◽  
Acquired Immunodeficiency Syndrome ◽  
Highly Active Antiretroviral Therapy ◽  
Immune Modulation ◽  
Pneumocystis Pneumonia ◽  
Sub Saharan Africa ◽  
Predisposing Factor ◽  
Acquired Immunodeficiency ◽  
Sub Saharan ◽  
Immunodeficiency Syndrome

Sub-Saharan Africa is the region of the world with the highest prevalence of helminth infections. To protect themselves from the defensive mechanisms of their respective hosts, helminths modulate their immune responses. This modulation has relevant clinical and epidemiological consequences, including the inhibition of inflammatory processes that characterize infection by other microorganisms. Severe Pneumocystis pneumonia is characterized by an intense inflammatory reaction that can lead to death. Acquired immunodeficiency syndrome is the main predisposing factor to the development of pneumocystosis. Although the introduction of highly active antiretroviral therapy has led to a notable decline in the incidence of acquired immunodeficiency syndrome-associated complications, pneumocystosis continues to be an important global health problem. Despite the high incidence of human immunodeficiency virus infection in the sub-Saharan region, the prevalence of Pneumocystis pneumonia there has been lower than expected. Several factors, or combinations thereof, may contribute to this evolution. Here, we hypothesize the possible role of helminth immune modulation as an important issue at play. On the other hand, and looking ahead, we believe that the immune modulation achieved by helminths may be an important factor to consider during the design and evaluation processes of vaccines against Pneumocystis jirovecii to be used in Sub-Saharan Africa. The requirements of a balanced triggering of different types of immune responses for controlling the infection produced by this microorganism, as observed during experiments in animal models, support this final consideration.

Evidence for Involvement of Transforming Growth Factor β1 Signaling Pathway in Activation of JC Virus in Human Immunodeficiency Virus 1–Associated Progressive Multifocal Leukoencephalopathy

2004 ◽  
Vol 128 (3) ◽  
pp. 282-291
Author(s):  
Sahnila Enam ◽  
Thersa M. Sweet ◽  
Shohreh Amini ◽  
Kamel Khalili ◽  
Luis Del Valle
Keyword(s):  
Human Immunodeficiency Virus ◽  
Growth Factor ◽  
Progressive Multifocal Leukoencephalopathy ◽  
Transforming Growth Factor ◽  
Jc Virus ◽  
Transforming Growth Factor Β1 ◽  
Immunodeficiency Virus ◽  
Acquired Immunodeficiency ◽  
Immunodeficiency Syndrome ◽  
Human Immunodeficiency Virus 1

Abstract Context.—Progressive multifocal leukoencephalopathy is a fatal demyelinating disease of the central nervous system frequently seen in patients with impaired immune systems, particularly acquired immunodeficiency syndrome. JC virus (JCV), a human neurotropic polyomavirus, is the etiologic infectious agent of this disease. Objective.—The significantly higher incidence of progressive multifocal leukoencephalopathy in patients with acquired immunodeficiency syndrome than in patients with other immunosuppressive conditions suggests that molecular interactions between human immunodeficiency virus 1 and JCV, via the Tat protein, are responsible for the activation of the JCV enhancer/promoter and the development of progressive multifocal leukoencephalopathy. An indirect mechanism through activation of cytokines, such as transforming growth factor β1 and Smads 3 and 4, may also be responsible for the enhancement of JCV gene expression. Design.—Immunohistochemical analysis in progressive multifocal leukoencephalopathy samples and chloramphenicol acetyl transferase assays on cell cultures were performed to corroborate this hypothesis. Results.—The JCV capsid protein VP-1 was found in the nuclei of oligodendrocytes and in the nuclei and cytoplasm of bizarre astrocytes. Human immunodeficiency virus proteins, including p24 and Tat, were detected in the cytoplasm of astrocytes. Tat, but not p24, was detected in oligodendrocytes, suggesting that extracellular Tat accumulates in the nuclei of oligodendrocytes, where JCV gene transcription takes place. High levels of transforming growth factor β1 and Smads 3 and 4 were detected in JCV-infected oligodendrocytes. Results from in vitro studies confirm activation of the JCV early and late promoters by Smads 3 and 4. Conclusions.—These observations support our model, suggesting that the induction of transforming growth factor β1 by human immunodeficiency virus 1 Tat can stimulate its downstream factors, including Smads 3 and 4, which in turn augment transcription of the JCV promoter in glial cells.

scholarly journals Analysis of HIV/AIDS Epidemic and Socioeconomic Factors in Sub-Saharan Africa

Entropy ◽  
2020 ◽  
Vol 22 (11) ◽  
pp. 1230 ◽  
Author(s):  
Shuman Sun ◽  
Zhiming Li ◽  
Huiguo Zhang ◽  
Haijun Jiang ◽  
Xijian Hu
Keyword(s):  
Socioeconomic Factors ◽  
Regression Models ◽  
Sub Saharan Africa ◽  
Likelihood Method ◽  
Unknown Parameters ◽  
Aids Epidemic ◽  
Acquired Immunodeficiency ◽  
Sub Saharan ◽  
Immunodeficiency Syndrome ◽  
Hiv Aids

Sub-Saharan Africa has been the epicenter of the outbreak since the spread of acquired immunodeficiency syndrome (AIDS) began to be prevalent. This article proposes several regression models to investigate the relationships between the HIV/AIDS epidemic and socioeconomic factors (the gross domestic product per capita, and population density) in ten countries of Sub-Saharan Africa, for 2011–2016. The maximum likelihood method was used to estimate the unknown parameters of these models along with the Newton–Raphson procedure and Fisher scoring algorithm. Comparing these regression models, there exist significant spatiotemporal non-stationarity and auto-correlations between the HIV/AIDS epidemic and two socioeconomic factors. Based on the empirical results, we suggest that the geographically and temporally weighted Poisson autoregressive (GTWPAR) model is more suitable than other models, and has the better fitting results.

Acquired Immunodeficiency Syndrome in African Patients

1984 ◽  
Vol 310 (8) ◽  
pp. 492-497 ◽  
Author(s):  
Nathan Clumeck ◽  
Jean Sonnet ◽  
Henri Taelman ◽  
Françoise Mascart-Lemone ◽  
Marc De Bruyere ◽  
...  
Keyword(s):  
Acquired Immunodeficiency Syndrome ◽  
Acquired Immunodeficiency ◽  
African Patients ◽  
Immunodeficiency Syndrome
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