scholarly journals Age‐Related Immune Dysfunction in Health and in Human Immunodeficiency Virus (HIV) Disease: Association of Age and HIV Infection with Naive CD8+Cell Depletion, Reduced Expression of CD28 on CD8+Cells, and Reduced Thymic Volumes

2003 ◽  
Vol 187 (12) ◽  
pp. 1924-1933 ◽  
Author(s):  
Robert C. Kalayjian ◽  
Alan Landay ◽  
Richard B. Pollard ◽  
Dennis D. Taub ◽  
Barry H. Gross ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Hiv Infection ◽  
Immune Dysfunction ◽  
Disease Association ◽  
Cell Depletion ◽  
Hiv Disease ◽  
Cd8 Cells ◽  
Age Related ◽  
Immunodeficiency Virus ◽  
Cd8 Cell

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....

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.

scholarly journals Rapid Onset of Intestinal Epithelial Barrier Dysfunction in Primary Human Immunodeficiency Virus Infection Is Driven by an Imbalance between Immune Response and Mucosal Repair and Regeneration

2007 ◽  
Vol 82 (1) ◽  
pp. 538-545 ◽  
Author(s):  
Sumathi Sankaran ◽  
Michael D. George ◽  
Elizabeth Reay ◽  
Moraima Guadalupe ◽  
Jason Flamm ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cell ◽  
Hiv Infection ◽  
Viral Replication ◽  
Cell Depletion ◽  
Epithelial Barrier ◽  
T Cell Depletion ◽  
Primary Hiv Infection ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT Gut-associated lymphoid tissue (GALT) is an early target for human immunodeficiency virus type 1 (HIV-1) infection and is a site for severe CD4+ T-cell depletion. HIV-associated enteropathy is well-documented in chronic HIV-1 infection. However, the initial host responses to HIV infection in GALT and the early molecular correlates of HIV enteropathogenesis have not been characterized during primary HIV infection. In this study, we provide evidence of viral replication in GALT resident CD4+ T cells and macrophages in primary-stage patients and identify early patterns of host mucosal responses and changes in the molecular microenvironment through gene expression profiling. High levels of viral replication in GALT and marked CD4+ T-cell depletion correlated with decreased expression levels of genes regulating epithelial barrier maintenance and digestive/metabolic functions. These changes coincided with a marked increase in the transcription of immune activation-, inflammation-, and apoptosis-associated genes. Our findings indicate that HIV-induced pathogenesis in GALT emerges at both the molecular and cellular levels prior to seroconversion in primary HIV infection, potentially setting the stage for disease progression by impairing the ability to control viral replication and repair and regenerate intestinal mucosal tissues.

scholarly journals Distribution and Evolution of T-Cell Receptor Vβ Repertoire on Peripheral Blood Lymphocytes of Newborn Infants of Human Immunodeficiency Virus (HIV)-Infected Mothers: Differential Display on CD4 and CD8 T Cells and Effect of HIV Infection

2007 ◽  
Vol 14 (9) ◽  
pp. 1215-1222 ◽  
Author(s):  
William Borkowsky ◽  
Song-He Chen ◽  
Ilana Belitskaya-Levy
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cell ◽  
Hiv Infection ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Peripheral Blood Mononuclear ◽  
Cd8 Cells ◽  
Significant Difference ◽  
Immunodeficiency Virus

ABSTRACT Neonatal human peripheral blood mononuclear cells from 12 human immunodeficiency virus (HIV)-infected and 84 uninfected children were assessed for their distribution of T-cell receptors (TCRs) by flow cytometry employing monoclonal antibodies to 14 Vβ types. Vβ 2, 5c, and 13 were the most commonly found on CD4 cells (in that order). There was a bimodal distribution of Vβ 2, being most common in 48% of individuals but in limiting frequency (<2% of CD4) in 21%. Vβ 2, 3, 8b, and 13 were most commonly expressed on CD8 cells at similar frequencies. There was little difference in the pattern displayed among the infected compared to that of the uninfected. The variation of the distribution over time was studied in 12 infants (7 infected). Only a single HIV-infected child had a significant difference in the interquartile range; none of the HIV-negative patients showed a significant difference. In conclusion, newborns demonstrate different distributions of TCR Vβ types on CD4 and CD8 cells. HIV infection produces no change in neonatal TCR and little change over the course of 2 years compared to that seen in the uninfected.

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.

scholarly journals CD4+ T Cell Depletion in Human Immunodeficiency Virus (HIV) Infection: Role of Apoptosis

Viruses ◽  
2011 ◽  
Vol 3 (5) ◽  
pp. 586-612 ◽  
Author(s):  
Michèle Février ◽  
Karim Dorgham ◽  
Angelita Rebollo
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cell ◽  
Hiv Infection ◽  
Cd4 T Cell ◽  
Cell Depletion ◽  
T Cell Depletion ◽  
Immunodeficiency Virus

scholarly journals Viral Interactions in Human Lymphoid Tissue: Human Herpesvirus 7 Suppresses the Replication of CCR5-Tropic Human Immunodeficiency Virus Type 1 via CD4 Modulation

2006 ◽  
Vol 81 (2) ◽  
pp. 708-717 ◽  
Author(s):  
Andrea Lisco ◽  
Jean-Charles Grivel ◽  
Angélique Biancotto ◽  
Christophe Vanpouille ◽  
Francesco Origgi ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Hiv Infection ◽  
Lymphoid Tissue ◽  
Human Herpesvirus ◽  
Hiv Disease ◽  
Immunodeficiency Virus ◽  
Human Lymphoid Tissue ◽  
Hiv 1

ABSTRACT Human immunodeficiency virus (HIV) infection is often accompanied by infection with other pathogens that affect the clinical course of HIV disease. Here, we identified another virus, human herpesvirus 7 (HHV-7) that interferes with HIV type 1 (HIV-1) replication in human lymphoid tissue, where critical events of HIV disease occur. Like the closely related HHV-6, HHV-7 suppresses the replication of CCR5-tropic (R5) HIV-1 in coinfected blocks of human lymphoid tissue. Unlike HHV-6, which affects HIV-1 by upregulating RANTES, HHV-7 did not upregulate any CCR5-binding chemokine. Rather, the inhibition of R5 HIV-1 by HHV-7 was associated with a marked downregulation of CD4, the cellular receptor shared by HHV-7 and HIV-1. HHV-7-induced CD4 downregulation was sufficient for HIV-1 inhibition, since comparable downregulation of CD4 with cyclotriazadisulfonamide, a synthetic macrocycle that specifically modulates expression of CD4, resulted in the suppression of HIV infection similar to that seen in HHV-7-infected tissues. In contrast to R5 HIV-1, CXCR4-tropic (X4) HIV-1 was only minimally suppressed by HHV-7 coinfection. This selectivity in suppression of R5 and X4 HIV-1 is explained by a suppression of HHV-7 replication in X4- but not in R5-coinfected tissues. These results suggest that HIV-1 and HHV-7 may interfere in lymphoid tissue in vivo, thus potentially affecting the progression of HIV-1 disease. Knowledge of the mechanisms of interaction of HIV-1 with HHV-7, as well as with other pathogens that modulate HIV-1 replication, may provide new insights into HIV pathogenesis and lead to the development of new anti-HIV therapeutic strategies.

ACQUIRED IMMUNODEFICIENCY SYNDROME, HUMAN IMMUNODEFICIENCY VIRUS AND HEMOPHILIA

1987 ◽  
Author(s):  
P H Levine
Keyword(s):  
United States ◽  
Human Immunodeficiency Virus ◽  
Hiv Infection ◽  
Specific Activity ◽  
Subsequent Development ◽  
Immune Dysfunction ◽  
The United States ◽  
Clotting Factor ◽  
Increased Risk ◽  
Immunodeficiency Virus

Less than 15 years ago the National Heart, Lung and Blood Institute surveyed physicians in the United States in order to characterize the demographics of hemophilia. The average age of persons with hemophilia in the United States was found to be 11.5 years old. By 10 years later, the life expectancy was predicted to be normal, and indeed the average age of persons with hemophilia in the U.S. is now in the early twenties. Early, intensive and predictably efficacious control of hemorrhage has made this result possible, and the therapeutic product which has allowed such control is commercial clotting factor concentrate.We now know that starting in 1978, and with great frquency during 1982 and 1983, the majority of U.S. hemophiliacs were infected with human immunodeficiency virus (HIV). It is estimated that as of January, 1987, approximately two thirds of the 20,000' persons with hemophilia in the United States have been infected with HIV. Among those with severe factor VIII deficiency, more than 9056 are seropositive. As of 1/5/87, there were 288 cases of AIDS among U.S. hemophiliacs, for an AIDS rate of approximately 2.256 of those with HIV infection. This number included 185 with severe, 32 with moderate and 28 with mild hemophilia A; 12 with severe, 6 with moderate and 1 with mild hemophilia B; 9 with vWD, and 4 others. A disproportionate number were older patients: 55 were ages 1-19; 62 ages 20-29; 85 ages 30-39, and 86 age 40 or older. Although the AIDS attack rate is no longer climbing logarhythmically, new cases are certainly still occurring.A variety of other HIV-related syndromes have emerged. Of great concern is immune thrombocytopenia, which is now relatively common; among a group of 209 carefully followed HIV-positive patients at our center, 31 (1556) are or have been thrombocytopenic. Progressive failure to normally gain height and weight in children with hemophilia has recently been shown by our group to correlate with HIV antibody positivity, and also with decreased T4/T8 ratio, decreased T4 cell count, decreased skin test reactivity, and subsequent development of ARC or AIDS in some such children. Finally, a picture of progressive fall in T4 count associated with recurrent non-specific infections and increased likelihood of positive viral culture, may predict an increased risk of developing AIDS.We know that the immune dysfunction in hemophilia is complex, and not wholly explained by HIV infection. One important factor may be the many foreign proteins contained in commercial clotting factor concentrates, and their ability to stimulate T cells. It is known that latent HIV infection in cultured T4 lymphocytes can be induced to enter the proliferative, viral secretory phase by the addition of soluble foreign antigens to the cell culture. Recent data of Brettler and colleagues, to be presented at this meeting, suggest that the use of highly purified VI!I:C (specific activity >3000 u/mg) in place of the present extremely impure products, may improve the immune dysfunction in hemophilia. This observation offers a new hypothetical approach to the prevention of progressive T4 cell depletion in HIV infected hemophiliacs, and requires immediate and extensive further study.The psychosocial burden of HIV infection is immense. The need for extensive, formal education and support programs is largely unmet in most parts of the world. Such programs are best run out of hemophilia treatment centers in most cases, and must include an active program on prevention of sexual transmission, provision of HIV testing before and during pregnancies, provision for maintenance of confidentiality, etc. Education concerning HIV is like all other forms of education. It requires formal organization, a curriculum, active rather than passive learning in which there is interaction between the teacher and the pupil, time for planned repetition, reinforcement with written materials, and assessment of goals achieved. For all of these reasons it is inappropriate to assume that the physician at the hemophilia center will be able to provide an adequate education program. Adquate paramedical personnel will need to undertake this effort, under the directjon of the physician.

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