Production of Interleukin-4, Interferon (IFN)-gamma and IFN-alpha in Human Immunodeficiency Virus-1 Infection: An Imbalance of Type 1 and Type 2 Cytokines may Reduce the Synthesis of IFN-alpha

1998 ◽  
Vol 48 (4) ◽  
pp. 436-442 ◽  
Author(s):  
Hober ◽  
Benyoucef ◽  
Chehadeh ◽  
Chieux ◽  
De La Tribonniere ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Interleukin 4 ◽  
Ifn Gamma ◽  
Ifn Alpha ◽  
Type 2 Cytokines ◽  
Immunodeficiency Virus ◽  
Human Immunodeficiency Virus 1

scholarly journals Coinfection with Schistosoma mansoni Reactivates Viremia in Rhesus Macaques with Chronic Simian-Human Immunodeficiency Virus Clade C Infection

2007 ◽  
Vol 75 (4) ◽  
pp. 1751-1756 ◽  
Author(s):  
Mila Ayash-Rashkovsky ◽  
Agnès-Laurence Chenine ◽  
Lisa N. Steele ◽  
Sandra J. Lee ◽  
Ruijiang Song ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Viral Replication ◽  
Schistosoma Mansoni ◽  
Rhesus Macaques ◽  
Cell Subset ◽  
Interleukin 4 ◽  
Immunodeficiency Virus ◽  
Clade C

ABSTRACT We tested the hypothesis that helminth parasite coinfection would intensify viremia and accelerate disease progression in monkeys chronically infected with an R5 simian-human immunodeficiency virus (SHIV) encoding a human immunodeficiency virus type 1 (HIV-1) clade C envelope. Fifteen rhesus monkeys with stable SHIV-1157ip infection were enrolled into a prospective, randomized trial. These seropositive animals had undetectable viral RNA and no signs of immunodeficiency. Seven animals served as virus-only controls; eight animals were exposed to Schistosoma mansoni cercariae. From week 5 after parasite exposure onward, coinfected animals shed eggs in their feces, developed eosinophilia, and had significantly higher mRNA expression of the T-helper type 2 cytokine interleukin-4 (P = 0.001) than animals without schistosomiasis. Compared to virus-only controls, viral replication was significantly increased in coinfected monkeys (P = 0.012), and the percentage of their CD4+ CD29+ memory cells decreased over time (P = 0.05). Thus, S. mansoni coinfection significantly increased viral replication and induced T-cell subset alterations in monkeys with chronic SHIV clade C infection.

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.

Acute Sexually Transmitted Infections Increase Human Immunodeficiency Virus Type 1 Plasma Viremia, Increase Plasma Type 2 Cytokines, and Decrease CD4 Cell Counts

2000 ◽  
Vol 182 (2) ◽  
pp. 459-466 ◽  
Author(s):  
Aggrey O. Anzala ◽  
J. Neil Simonsen ◽  
Joshua Kimani ◽  
T. Blake Ball ◽  
Nico J. D. Nagelkerke ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Plasma Viremia ◽  
Sexually Transmitted ◽  
Cell Counts ◽  
Cd4 Cell Counts ◽  
Type 2 Cytokines ◽  
Immunodeficiency Virus ◽  
Cd4 Cell

scholarly journals A Balanced Type 1/Type 2 Response Is Associated with Long-Term Nonprogressive Human Immunodeficiency Virus Type 1 Infection

2002 ◽  
Vol 76 (18) ◽  
pp. 9011-9023 ◽  
Author(s):  
Nesrina Imami ◽  
Antonio Pires ◽  
Gareth Hardy ◽  
Jamie Wilson ◽  
Brian Gazzard ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Interleukin 4 ◽  
Wide Range ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT Previous reports have emphasized the requirements for strong type 1 cell-mediated responses in the control of human immunodeficiency virus type 1 (HIV-1). HIV-1 Gag p24-specific CD4 helper T-lymphocyte (HTL) responses have been shown to inversely correlate with viral burden in HIV-1-infected individuals. In this study, peripheral blood mononuclear cells from 70 individuals with chronic progressive HIV-1 infection (clinical progressors), 10 clinical nonprogressors, and 3 immunologically discordant progressors were assessed for HTL proliferation and type 1/type 2 cytokine production. Clinical progressors lacked functional HIV-1-specific HTLs with proliferative and cytokine-producing capacity. Clinical nonprogressors were found to respond to a wide range of HIV-1 antigens from different clades, producing both type 1 and type 2 cytokines. Immunologically discordant progressors responded strongly to clade B Gag p24 with a type 1 cytokine profile but not to other antigens. Thus, in contrast to clinical nonprogressors, neither progressors nor immunologically discordant progressors secreted interleukin-4 (IL-4) in response to HIV-1 antigens. Both clinical nonprogressors and immunologically discordant progressors responded broadly to B clade Gag p24-overlapping peptides. However, IL-4 production in the nonprogressors was restricted to a limited number of p24 peptides. No HIV-1-specific T-cell responses were seen in 20 seronegative controls. Additionally, we observed a rapid type 1 to type 2 shift in the response of one immunologically discordant progressor upon onset of clinical symptoms. These results suggest that a balanced type 1/type 2 profile correlates with successful long-term control of HIV-1.

scholarly journals Effects of the Th1 and Th2 stimulatory cytokines interleukin-12 and interleukin-4 on human immunodeficiency virus replication

Blood ◽  
1995 ◽  
Vol 85 (8) ◽  
pp. 2114-2123 ◽  
Author(s):  
A Foli ◽  
MW Saville ◽  
MW Baseler ◽  
R Yarchoan
Keyword(s):  
Human Immunodeficiency Virus ◽  
Mononuclear Cells ◽  
Interleukin 4 ◽  
Interleukin 12 ◽  
Human Immunodeficiency Virus Replication ◽  
Hiv Replication ◽  
Peripheral Blood Mononuclear ◽  
Immunodeficiency Virus

The cytokines interleukin-12 (IL-12) and IL-4 play important roles in the development of Th1-like (type-1) and Th2-like (type-2) T-cell responses, respectively, and there is evidence that type-1/type-2 T helper imbalances are important in the pathogenesis of human immunodeficiency virus (HIV) disease. With this background, we examined the effects of these cytokines on HIV replication. Neither stimulated HIV replication in fresh peripheral blood mononuclear cells (PBMC). However, in prestimulated PBMC, IL-12, and to a greater extent, IL-4 as well as IL-2, induced production of HIV p24 antigen over 7 days of culture (no cytokine 3,900 x/divided by 1.31 [GM x/divided by SEM] pg/mL; IL-12, 34,300 x/divided by 1.39 pg/mL; IL-4, 283,000 x/divided by 1.14 pg/mL; and IL-2, 328,000 x/divided by 1.31 pg/mL). Neither IL-12- nor IL-4-induced HIV replication was attributable to induction of IL-1, IL-2, tumor necrosis factor (TNF)-alpha, or TNF-beta. Both IL-12- and IL-4-induced HIV replication was associated with selective loss of the CD4+ subset in stimulated cultures. IL-4 stimulated HIV replication in monocyte/macrophages, while IL-12 had little or no effect in these cells. Finally, HIV replication stimulated by IL-12 or IL-4 was inhibited by dideoxynucleosides. Thus, IL-12 and IL-4 enhance HIV replication and HIV-induced cell death in prestimulated PBMC. Through killing of the CD4+ T cells stimulated by these cytokines, this may result in inappropriate type-1/type-2 responses in HIV-infected patients and contribute to their Th1 immunodeficiency.

scholarly journals Human immunodeficiency virus types 1 and 2 have different replication kinetics in human primary macrophage culture

2006 ◽  
Vol 87 (2) ◽  
pp. 411-418 ◽  
Author(s):  
David Marchant ◽  
Stuart J. D. Neil ◽  
Áine McKnight
Keyword(s):  
Human Immunodeficiency Virus ◽  
Mononuclear Cells ◽  
Peripheral Blood Mononuclear ◽  
Steady Rate ◽  
Immunodeficiency Virus ◽  
Load Characteristics ◽  
Kinetics Of ◽  
Hiv 1

This study compares the replication of primary isolates of human immunodeficiency virus type 2 (HIV-2) and type 1 (HIV-1) in monocyte-derived macrophages (MDMs). Eleven HIV-2 and five HIV-1 primary isolates that use CCR5, CXCR4 or both coreceptors to enter cells were included. Regardless of coreceptor preference, 10 of 11 HIV-2 viruses could enter, reverse transcribe and produce fully infectious virus in MDMs with efficiency equal to that in peripheral blood mononuclear cells. However, the kinetics of replication of HIV-2 compared with HIV-1 over time were distinct. HIV-2 had a burst of virus replication 2 days after infection that resolved into an apparent ‘latent state’ at day 3. HIV-1, however, continued to produce infectious virions at a lower, but steady, rate throughout the course of infection. These results may have implications for the lower pathogenesis and viral-load characteristics of HIV-2 infection.

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