scholarly journals Effect of co-morbidities on disease course in human immunodeficiency virus-infected illicit drug users in the era of highly active antiretroviral therapy

2015 ◽  
Vol 37 ◽  
pp. e2015008
Author(s):  
Venkataramana Kandi
Keyword(s):  
Human Immunodeficiency Virus ◽  
Antiretroviral Therapy ◽  
Highly Active Antiretroviral Therapy ◽  
Drug Users ◽  
Illicit Drug ◽  
Disease Course ◽  
Illicit Drug Users ◽  
Highly Active ◽  
Immunodeficiency Virus

scholarly journals Highly Active Antiretroviral Therapy Normalizes the Function of Progenitor Cells in Human Immunodeficiency Virus–Infected Patients

1998 ◽  
Vol 178 (5) ◽  
pp. 1299-1305 ◽  
Author(s):  
Susanne Dam Nielsen ◽  
Annette Kjær Ersbøll ◽  
Lars Mathiesen ◽  
Jens Ole Nielsen ◽  
John‐Erik Stig Hansen
Keyword(s):  
Human Immunodeficiency Virus ◽  
Antiretroviral Therapy ◽  
Progenitor Cells ◽  
Highly Active Antiretroviral Therapy ◽  
Highly Active ◽  
Immunodeficiency Virus

scholarly journals Highly Active Antiretroviral Therapy in Human Immunodeficiency Virus Type 1-Infected Children: Analysis of Cellular Immune Responses

2001 ◽  
Vol 8 (5) ◽  
pp. 943-948 ◽  
Author(s):  
Vesna Blazevic ◽  
Shirley Jankelevich ◽  
Seth M. Steinberg ◽  
Freda Jacobsen ◽  
Robert Yarchoan ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cell ◽  
Antiretroviral Therapy ◽  
Highly Active Antiretroviral Therapy ◽  
Delayed Type Hypersensitivity ◽  
Strong Increase ◽  
Highly Active ◽  
Cell Counts ◽  
Immunodeficiency Virus

ABSTRACT The present study analyzes the effect of highly active antiretroviral therapy (HAART) on restoration of cellular immunity in human immunodeficiency virus (HIV)-infected children over a 24-week period following initiation of HAART with ritonavir, nevirapine, and stavudine. The immunological parameters evaluated at four time points (at enrollment and at 4, 12, and 24 weeks of therapy) included cytokine production by monocytes as well as T-cell proliferation in response to mitogen, alloantigen, and recall antigens including HIV type 1 envelope peptides. Circulating levels of interleukin-16 (IL-16) were measured, in addition to CD4+ T-cell counts, plasma HIV RNA levels, and the delayed-type hypersensitivity (DTH) response. At enrollment the children exhibited defects in several immune parameters measured. Therapy increased CD4+ T-cell counts and decreased viral loads significantly. By contrast, the only immunological parameter that was significantly increased was IL-12 p70 production by monocytes; the DTH response to Candida albicans also showed a strong increase in patients becoming positive. In conclusion, these results demonstrate that HAART in HIV-infected children affects the dynamics of HIV replication and the CD4+ T-cell count over 24 weeks, similar to the pattern seen in HIV-infected adults. Furthermore, these data indicate improvement in antigen-presenting cell immunological function in HIV-infected children induced by HAART.

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