Interferon alpha (IFN)-Macrophage Interactions in Human Immunodeficiency Virus (HIV) Infection: Role of IFN in the Tempo and Progression of HIV Disease

1992 ◽  
Vol 8 (1) ◽  
pp. 43-54 ◽  
Author(s):  
Howard E. Gendelman ◽  
Donald R. Skillman ◽  
Monte S. Meltzer
Keyword(s):  
Human Immunodeficiency Virus ◽  
Hiv Infection ◽  
Interferon Alpha ◽  
Hiv Disease ◽  
Immunodeficiency Virus

Human Immunodeficiency Virus Hematology

Hematology ◽  
2003 ◽  
Vol 2003 (1) ◽  
pp. 294-313 ◽  
Author(s):  
Paul A. Volberding ◽  
Kelty R. Baker ◽  
Alexandra M. Levine
Keyword(s):  
Human Immunodeficiency Virus ◽  
Hiv Infection ◽  
Hiv Care ◽  
Hiv Disease ◽  
Secondary Infections ◽  
Antiretroviral Drug ◽  
Immunodeficiency Virus ◽  
History Of ◽  
Relationship Of

Abstract The advent of potent antiretroviral therapy has altered the expected natural history of human immunodeficiency virus (HIV) infection and of many previously associated opportunistic complications, including malignancies. At the same time, HIV suppression hasn’t affected all of these complications equally and the longer expected survival of infected patients may allow the development of newer complications. Additionally, the use of potent antiretroviral combination therapy may itself lead to hematological toxicities. Together these changes affect the consultation role of the hematology-oncology specialist in comprehensive HIV care and demand ongoing education. In Section I, Dr. Paul Volberding reviews the biology of antiretroviral drug development and the progression in discovering new agents as the viral life cycle is further elucidated. He briefly summarizes the process of combining agents to achieve the degree of viral suppression required for long-term clinical benefit. In Section II, Dr. Kelty Baker reviews the effects of HIV and its therapy on hematologic dyscrasia and clotting disorders. She summarizes how therapy may decrease certain previously common manifestations of HIV disease while adding new problems likely to result in referral to the hematologist. In addition, she addresses the role of secondary infections, such as parvovirus, in this spectrum of disorders. In Section III, Dr. Alexandra Levine discusses the still challenging aspects of HIV associated non-Hodgkin’s lymphoma and the association between HIV infection and Hodgkin’s disease. She addresses current controversies in the pathogenesis of HIV related lymphomas and summarizes a number of recent trials of combination chemotherapy, with or without monoclonal antibodies, in their management. Additionally, she reviews the complex relationship of HIV disease with multicentric Castleman’s disease and recent attempts to manage this disorder.

Human immunodeficiency virus (HIV) infection

2011 ◽  
pp. 663-669
Keyword(s):  
Human Immunodeficiency Virus ◽  
Hiv Infection ◽  
Opportunistic Infections ◽  
Tissue Loss ◽  
Atherosclerotic Cardiovascular Disease ◽  
Hiv Disease ◽  
Hiv Replication ◽  
Pharmacological Management ◽  
Nutritional Conditions ◽  
Immunodeficiency Virus

Introduction, nutritional goals, and assessment 664 Unintentional weight and lean tissue loss 666 Cardiovascular risk and complications associated with HIV disease and treatment 667 Additional dietary issues 668 Untreated human immunodeficiency virus (HIV) infection leads to progressive suppression of immune function, eventually rendering the body susceptible to opportunistic infections and tumours. While there is no cure, antiretroviral therapy (ART) is highly effective in suppressing HIV replication. HIV disease is now a chronic condition and causes of death in this population have shifted from traditional AIDS-related illnesses to non-AIDS (Acquired Immune Deficiency Syndrome) events, the most common being atherosclerotic cardiovascular disease, liver disease, end-stage renal disease and non-AIDS–defining malignancies. There are a diverse range of nutritional conditions associated with HIV, reflecting the complexity of the disease and pharmacological management....

Possible Role of Interleukin-10 (IL-10) and CD40 Ligand Expression in the Pathogenesis of Hypergammaglobulinemia in Human Immunodeficiency Virus Infection: Modulation of IL-10 and Ig Production After Intravenous Ig Infusion

Blood ◽  
1998 ◽  
Vol 92 (10) ◽  
pp. 3721-3729 ◽  
Author(s):  
Fredrik Müller ◽  
Pål Aukrust ◽  
Ingvild Nordøy ◽  
Stig S. Frøland
Keyword(s):  
Human Immunodeficiency Virus ◽  
Hiv Infection ◽  
Cd40 Ligand ◽  
Interleukin 10 ◽  
Lymphocyte Function ◽  
General Effect ◽  
Bolus Infusion ◽  
Single Bolus ◽  
Immunodeficiency Virus

Abstract The mechanisms leading to polyclonal hypergammaglobulinemia in patients with human immunodeficiency virus (HIV) infection are not well understood. In light of the important role of interleukin-10 (IL-10) and the interaction between CD40 and CD40 ligand in the normal regulation of B-lymphocyte function and Ig production, we examined these parameters in 24 HIV-infected patients. Both plasma IL-10 levels and the percentage of CD4+ and CD8+lymphocytes expressing CD40 ligand were significantly higher in the patients than in the 10 blood donor controls. Serum IgG correlated positively with circulating IL-10 levels and the percentage of CD4+ lymphocytes expressing CD40 ligand. Furthermore, a single bolus infusion of intravenous Ig (0.4 g/kg) in 8 HIV-infected patients caused a further increase in IL-10 levels in plasma and an increase in both IL-10 and IgG production in peripheral blood mononuclear cell cultures. In another patient group (Wegener’s granulomatosis) receiving a single bolus infusion of intravenous Ig, a similar increase in plasma IL-10 levels was found, suggesting that this may be a general effect of intravenous Ig. In patients with HIV infection, our data suggest that a vicious cycle may be operative where high endogenous Ig levels may enhance IL-10 production that, in turn, leads to higher Ig production.

Human Immunodeficiency Virus (HIV)-Resistant CD4+ UT-7 Megakaryocytic Human Cell Line Becomes Highly HIV-1 and HIV-2 Susceptible Upon CXCR4 Transfection: Induction of Cell Differentiation by HIV-1 Infection

Blood ◽  
1997 ◽  
Vol 89 (8) ◽  
pp. 2670-2678 ◽  
Author(s):  
Marta Baiocchi ◽  
Eleonora Olivetta ◽  
Cristiana Chelucci ◽  
Anna Claudia Santarcangelo ◽  
Roberta Bona ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Hiv Infection ◽  
Cell Line ◽  
Viral Entry ◽  
Human Cell Line ◽  
Immunodeficiency Virus ◽  
Hiv Entry ◽  
Stromal Cell Derived Factor ◽  
Hiv 1

Abstract Recent findings have shown that the expression of the seven trans-membrane G-protein–coupled CXCR4 (the receptor for the stromal cell-derived factor [SDF]-1 chemokine) is necessary for the entry of T-lymphotropic human immunodeficiency virus (HIV) strains, acting as a coreceptor of the CD4 molecule. In the human system, the role of CXCR4 in HIV infection has been determined through env-mediated cell fusion assays and confirmed by blocking viral entry in CD4+/CXCR4+ cells by SDF-1 pretreatment. We observed that the human megakaryoblastic CD4+ UT-7 cell line fails to express CXCR4 RNA and is fully resistant to HIV entry. Transfection of an expression vector containing the CXCR4 c-DNA rendered UT-7 cells readily infectable by different T-lymphotropic syncytium-inducing HIV-1 and HIV-2 isolates. Interestingly, HIV-1 infection of CXCR4 expressing UT-7 cells (named UT-7/fus) induces the formation of polynucleated cells through a process highly reminiscent of megakaryocytic differentiation and maturation. On the contrary, no morphologic changes were observed in HIV-2–infected UT-7/fus cells. These findings further strengthen the role of CXCR4 as a molecule necessary for the replication of T-lymphotropic HIV-1 and HIV-2 isolates and provide a useful model to study the functional role of CD4 coreceptors in HIV infection.

scholarly journals Isolation of Lautropia mirabilis from Oral Cavities of Human Immunodeficiency Virus-Infected Children

1998 ◽  
Vol 36 (6) ◽  
pp. 1756-1760 ◽  
Author(s):  
Susan Norton Rossmann ◽  
Patricia H. Wilson ◽  
John Hicks ◽  
Bruce Carter ◽  
Stanley G. Cron ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Oral Cavity ◽  
Hiv Infection ◽  
Clinical Status ◽  
Clinical Disease ◽  
Gram Negative ◽  
Immunological Status ◽  
Immunodeficiency Virus ◽  
Concomitant Factors

Lautropia mirabilis, a pleomorphic, motile, gram-negative coccus, has been isolated from the oral cavities of 32 of 60 (53.3%) children infected with human immunodeficiency virus (HIV) and 3 of 25 (12.0%) HIV-uninfected controls; the association ofL. mirabilis isolation with HIV infection is significant (P < 0.001). All children in the study, both HIV-infected children and controls, were born to HIV-infected mothers. The presence of this bacterium was not associated with clinical disease in these children. The HIV-infected children with L. mirabilis did not differ from the HIV-infected children withoutL. mirabilis in immunological status, clinical status, or systemic medications. The role of HIV infection itself or concomitant factors in the establishment of L. mirabilis in the oral cavity remains to be elucidated.

Role of Lymphoid Organs in the Pathogenesis of Human Immunodeficiency Virus (HIV) Infection

1994 ◽  
Vol 140 (1) ◽  
pp. 105-130 ◽  
Author(s):  
Giuseppe Pantaleo ◽  
Cecilia Graziosi ◽  
James F. Demarest ◽  
Oren J. Cohen ◽  
Mauro Vaccarezza ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Hiv Infection ◽  
Lymphoid Organs ◽  
Immunodeficiency Virus

scholarly journals The breakdown of the cytokine network subsequent to human immunodeficiency virus infection

1995 ◽  
Vol 4 (5) ◽  
pp. 315-321
Author(s):  
M. Clerici ◽  
M. L. Villa ◽  
D. Trabattoni ◽  
G. M. Shearer
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Lymphocytes ◽  
Hiv Infection ◽  
Hiv Disease ◽  
Cytokine Network ◽  
Type 2 Cytokines ◽  
Immunodeficiency Virus ◽  
Hiv Seropositive

The acquired immunodeflciency syndrome (AIDS) is a clinically multifaceted disease induced by infection with the human immunodeficiency virus (HIV). HIV infection results in a complex pattern of immunologic alterations that leads to the development of AIDS in the majority of HIV seropositive (HIV+) individuals. The reduction in CD4 T lymphocyte counts is the hallmark of HIV infection; nevertheless, long before the reduction in CD4 counts reaches critical levels, a series of profound and complex defects that impair the function of CD4 T lymphocytes can be detected. Thus, HIV infection is characterized by quantitative and qualitative defects affecting CD4 T lymphocytes. It was suggested recently that programmed cell death (PCD) is an important mechanism leading to CD4 depletion in HIV infection, and that susceptibility of peripheral lymphocytes to PCD is differentially regulated by diverse cytokines. Thus, type 1 cytokines would protect CD4 lymphocytes against PCD, whereas type 2 cytokines would not protect against, and could augment, PCD. We suggest that the qualitative alterations of the immune response provoke the CD4 depletion characteristic of HIV disease via type 2 cytokinemediated augmentation of PCD, and are therefore ultimately responsible for the progression of HIV infection. Finally, we summarize recent data showing that three correlates of disease progression: emergence of HIV strains with syncitium-inducing ability (SI), type 1-to-type 2 cytokine shift, and CD4 depletion, are significantly associated, suggesting a complex interconnected virologic-immunologic pathogenesis of HIV infection.

scholarly journals Markers predicting progression of human immunodeficiency virus-related disease.

1994 ◽  
Vol 7 (1) ◽  
pp. 14-28 ◽  
Author(s):  
C M Tsoukas ◽  
N F Bernard
Keyword(s):  
Human Immunodeficiency Virus ◽  
Immune System ◽  
Hiv Infection ◽  
Disease Progression ◽  
Opportunistic Infections ◽  
Surrogate Marker ◽  
Disease Process ◽  
Surrogate Markers ◽  
Hiv Disease ◽  
Immunodeficiency Virus

Human immunodeficiency virus (HIV) interacts with the immune system throughout the course of infection. For most of the disease process, HIV activates the immune system, and the degree of activation can be assessed by measuring serum levels of molecules such as beta 2-microglobulin and neopterin, as well as other serum and cell surface phenotype markers. The levels of some of these markers correlate with clinical progression of HIV disease, and these markers may be useful as surrogate markers for development of clinical AIDS. Because the likelihood and timing of development of clinical AIDS following seroconversion, for any particular individual, are not readily predictable, the use of nonclinical disease markers has become critically important to patient management. Surrogate markers of HIV infection are, by definition, measurable traits that correlate with disease progression. An ideal marker should identify patients at highest risk of disease progression, provide information on how long an individual has been infected, help in staging HIV disease, predict development of opportunistic infections associated with AIDS, monitor the therapeutic efficacy of immunomodulating or antiviral treatments, and the easily quantifiable, reliable, clinically available, and affordable. This review examines the current state of knowledge and the role of surrogate markers in the natural history and treatment of HIV infection. The clinical usefulness of each marker is assessed with respect to the criteria outlined for the ideal surrogate marker for HIV disease progression.

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