Mortality in hospitalized human immunodeficiency virus (HIV) and tuberculosis(TB) infection patients: zero inflated negative binomial death rate (ZINBDR) models

2013 ◽  
Vol 7 ◽  
pp. 37-47 ◽  
Author(s):  
Mohd Asrul A.A ◽  
Nyi Nyi Naing
Author(s):  
Michael B. A. Oldstone

This chapter explores acquired immunodeficiency syndrome (AIDS), a lethal disease cause by the human immunodeficiency virus (HIV). Of the more than 75 million people HIV has infected in the 36 years (1983–2019) since the initial case report, nearly one-half of them have died. Not only the victims of this infection but also their families, communities, countries, and even continents endured years of suffering as AIDS proceeded on its long course of physical destruction. Today, however, the enormous advance in antivirus drug therapy has dramatically reduced the death rate and altered the portrait of this disease from an acute lethal disease to a chronic persistent infection. In 2019, the combination antiretroviral therapy has enabled those infected to survive at roughly the same rate as the general non-infected population. However, this increased longevity includes an upsurge in the former group’s medical problems caused by the side effects of antiretroviral therapy. Despite an outlay of $1 billion per year for AIDS research, no vaccine is on the horizon for preventing this medical catastrophe.


1998 ◽  
Vol 16 (5) ◽  
pp. 1729-1735 ◽  
Author(s):  
M O Granovsky ◽  
B U Mueller ◽  
H S Nicholson ◽  
P S Rosenberg ◽  
C S Rabkin

PURPOSE To describe the spectrum of malignancies in human immunodeficiency virus (HIV)-infected children and the clinical outcome of patients with these tumors. METHODS We retrospectively surveyed the Children's Cancer Group (CCG) and the National Cancer Institute (NCI) for cases of cancer that occurred between July 1982 and February 1997 in children who were HIV seropositive before or at the time of cancer diagnosis. We used Kaplan-Meier survivorship curves, hazard function estimates, and Cox proportional hazards models to evaluate survival. RESULTS Sixty-four children (39 boys, 25 girls) with 65 tumors were reported. Thirty-seven children (58%) acquired HIV infection vertically (median age at cancer diagnosis, 4.3 years); 22 children (34%) acquired HIV through transfusion of blood or blood products (median age at cancer diagnosis, 13.4 years). Forty-two children (65%) had non-Hodgkin's lymphoma (NHL). Eleven children (17%) had leiomyosarcomas (or leiomyomas), which are otherwise exceptionally rare in children. Other malignancies included acute leukemia (five children), Kaposi's sarcoma (KS; three children), Hodgkin's disease (two children), vaginal carcinoma in situ (one child), and tracheal neuroendocrine carcinoma (one child). Median survival after NHL diagnosis was 6 months (range, 1 day to 89 months) and after leiomyosarcoma was 12 months (range, 10 days to 19 months). The average monthly death rate after NHL diagnosis was 12% in the first 6 months, which decreased to about 2% thereafter. In contrast, the monthly death rate after leiomyosarcoma diagnosis increased from 5% in the first 6 months to about 20% thereafter. CONCLUSION After NHL, leiomyosarcoma is the second leading cancer in children with HIV infection. Both cancers have high mortality rates; improved outcome for NHL, in particular, may depend on earlier diagnosis and therapy.


2005 ◽  
Vol 79 (7) ◽  
pp. 4025-4032 ◽  
Author(s):  
Christina Speirs ◽  
Erik van Nimwegen ◽  
Diane Bolton ◽  
Mihaela Zavolan ◽  
Melody Duvall ◽  
...  

ABSTRACT Human immunodeficiency virus (HIV) causes complex metabolic changes in infected CD4+ T cells that lead to cell cycle arrest and cell death by necrosis. To study the viral functions responsible for deleterious effects on the host cell, we quantitated the course of HIV type 1 infection in tissue cultures by using flow cytometry for a virally encoded marker protein, heat-stable antigen (HSA). We found that HSA appeared on the surface of the target cells in two phases: passive acquisition due to association and fusion of virions with target cells, followed by active protein expression from transcription of the integrated provirus. The latter event was necessary for decreased target cell viability. We developed a general mathematical model of viral dynamics in vitro in terms of three effective time-dependent rates: those of cell proliferation, infection, and death. Using this model we show that the predominant contribution to the depletion of viable target cells results from direct cell death rather than cell cycle blockade. This allows us to derive accurate bounds on the time-dependent death rates of infected cells. We infer that the death rate of HIV-infected cells is 80 times greater than that of uninfected cells and that the elimination of the vpr protein reduces the death rate by half. Our approach provides a general method for estimating time-dependent death rates that can be applied to study the dynamics of other viruses.


1987 ◽  
Vol 1 (3) ◽  
pp. 381-395 ◽  
Author(s):  
Beverly Ryan ◽  
Edward Connor ◽  
Anthony Minnefor ◽  
Frank Desposito ◽  
James Oleske

2001 ◽  
Vol 36 (3) ◽  
pp. 225-234
Author(s):  
Ramazan Idilman ◽  
Alessandra Colantoni ◽  
Nicola De Maria ◽  
James M. Harig ◽  
David H. van Thiel

VASA ◽  
2015 ◽  
Vol 44 (5) ◽  
pp. 387-390
Author(s):  
Thomas Kotsis ◽  
Louizos-Alexandros Louizos ◽  
Spyridon Mylonas ◽  
Evangelos Pappas ◽  
Karandrea Despoina ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document