HIV-I and HIV-2 isolates differ in their ability to activate the complement system on the surface of infected cells

Marschang, Peter; Gürtler, Leo; Tötsch, Martin; Thielens, Nicole M.; Gj, Arlaud; Hittmair, A; Katinger, Hermann; Mp, Dierich

doi:10.1097/00002030-199307000-00001

Cited by 34 publications

(19 citation statements)

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“…Virus inactivation through opsonization and lysis has been reported to dominate when the expression of CRPs on the HIV-1 envelope is limited, whereas the presence of CRs on the target cells may enhance viral infectivity (21)(22)(23). With just two exceptions (24,25), it should be noted that little is known on the role of complement in HIV-2 infection.…”

mentioning

confidence: 99%

Effect of Complement on HIV-2 Plasma Antiviral Activity Is Intratype Specific and Potent

Şahin

Holmgren

Sheik-Khalil

et al. 2013

J Virol

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Human immunodeficiency virus type 2 (HIV-2)-infected individuals develop immunodeficiency with a considerable delay andtransmit the virus at rates lower than HIV-1-infected persons. Conceivably, comparative studies on the immune responsiveness of HIV-1-and HIV-2-infected hosts may help to explain the differences in pathogenesis and transmission between the two types of infection. Previous studies have shown that the neutralizing antibody response is more potent and broader in HIV-2 than in HIV-1 infection. In the present study, we have examined further the function of the humoral immune response and studied the effect of complement on the antiviral activity of plasma from singly HIV-1-or HIV-2-infected individuals, as well as HIV-1/ HIV-2 dually infected individuals. The neutralization and antibody-dependent complement-mediated inactivation of HIV-1 and HIV-2 isolates were tested in a plaque reduction assay using U87.CD4.CCR5 cells. The results showed that the addition of complement increased intratype antiviral activities of both HIV-1 and HIV-2 plasma samples, although the complement effect was more pronounced with HIV-2 than HIV-1 plasma. Using an area-under-the-curve (AUC)-based readout, multivariate statistical analysis confirmed that the type of HIV infection was independently associated with the magnitude of the complement effect. The analyses carried out with purified IgG indicated that the complement effect was largely exerted through the classical complement pathway involving IgG in both HIV-1 and HIV-2 infections. In summary, these findings suggest that antibody binding to HIV-2 structures facilitates the efficient use of complement and thereby may be one factor contributing to a strong antiviral activity present in HIV-2 infection.

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confidence: 99%

Effect of Complement on HIV-2 Plasma Antiviral Activity Is Intratype Specific and Potent

Şahin

Holmgren

Sheik-Khalil

et al. 2013

J Virol

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“…Previous reports of "antibody-independent" C activation by HIV and HIV-infected cells were made by Solder et al [26] and Marschang et al [9]. These investigators observed that various laboratory isolates of HIV and.…”

Section: Discussionmentioning

confidence: 98%

“…but not by HIV-infected cells, since they activated the alternative pathway. Despite this discrepancy, the investigators attributed the mechanism of C activation by infected cells to sites on gp4l which become exposed, probably during binding of gpl20 to CD4 [9].…”

Section: Discussionmentioning

confidence: 99%

“…Peptides representing amino acid region 590 613 of gpl60 (an external immunodominant area of gp4I) were shown to compete with Clq for binding to solid-phase gp41 [8]. The same group showed that "antibody-independent" C activation by infected H9 cells was highly variable depending on the HIV isolate [9]. The reason for this variability was attributed to the possible masking of the gp4I molecule by gpl20 or the shedding of gp 120 after possible CD4 binding.…”

Section: Introductionmentioning

confidence: 99%

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Efficacy of HIV-specific and ‘antibody-independent’ mechanisms for complement activation by HIV-infected cells

Saarloos¹,

Lint²,

Spear³

1995

Clinical and Experimental Immunology

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SUMMARYPrevious studies in this laboratory have shown that efficient activation of complement (C) on HIV isolates and HIV-infected cells requires the binding of specific anii-HIV antibodies, while other investigators have observed "antibody-independent' C activation. In an attempt to clarify these disparate findings, we investigated the effect of several variables on C activation by HIV-infected cells using flow cytometric analysis of C3 deposition. Antibody-mediated C activation using pooled sera from infected persons or human MoAbs directed against the V3 region of gpl20 was always substantially higher than activation without antibody. Normal human serum (NHS) from a subset of HIV antibody-negative donors did. however, induce low levels of C3 deposilion. Differences in C3 activation between the various NHS did not correlate with total haemolytic C levels or mannose-binding protein (MBP) levels. IgM isolated from NHS that induced high levels of C activation was at least partly responsible for the 'antibody-independent* C activation. Although there appeared to be a correlation between NHS that induced C activation and the presence of anti-blood type B IgM. absorption of anti-B did not abrogate the C3 deposition. Additionally. MoAb to the B antigen did not induce C3 deposition. These studies show that IgM in sera from HI V-uninfected donors can induce C3 deposition on HIV-infected cells, but that specific anti body-dependent C activation is substantially more efficient. Therefore, "antibody-independent' C activation on HIV-infected cells may. in some cases, be more accurately described as HI V-crossreactive antibody-dependent C activation.

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“…HIV-infected cells trigger both the alternative and the classical pathway [4][5][6]. Despite some observations suggesting that human serum may affect HIV infectivity in the presence of specific antibodies [7,8], the role of complement together with anti-HIV antibodies for virus inactivation is not yet clarified.…”

Section: Introductionmentioning

confidence: 99%

Complement-dependent cytotoxic antibodies to human T lymphotropic virus type I (HTLV-I)-infected cells in the sera of HTLV-I-infected individuals

Plotnicky-Gilquin

Afani

et al. 1996

Clinical and Experimental Immunology

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To investigate whether HTLV‐I induces the development of complement‐dependent cytotoxic antibodies in humans, sera of asymptomatic HTLV‐I carriers and of patients suffering from tropical spastic paraparesis/HTLV‐I‐associated myelopathy (TSP/HAM) or adult T cell leukaemia (ATL) were used in a cytotoxicity assay against a panel of target cells. This panel included uninfected cell lines (CEM, Jurkat, Molt and H9), cell lines chronically infected with HTLV‐I (MT2, MT4, C91PL and HUT102), as well as lines H36 (H9 infected with HTLV‐I), H9‐IIIB (H9 infected with HIVIIIB) and H9‐MN (H9 infected with HIVMN). HTLV‐I+ sera induced lysis of H36 and of lines expressing HTLV‐I antigens in the presence of rabbit complement, but did not lyse cells in presence of human complement. The HTLV‐I+ sera also failed to lyse the HTLV‐I− lines and H9 cells, suggesting that lysis was specific for HTLV‐I. H36 cell lysis was prevented by IgG depletion of the sera and by dialysis of rabbit complement against EGTA or EDTA. Rabbit complement‐dependent cytotoxic antibodies were present in the sera of 14/14 HTLV‐I‐infected individuals; the highest titres were predominantly found in the sera of the TSP/HAM patients. Such antibodies were also detected in 5/5 individuals coinfected with HIV‐1 and HTLV‐I, although no cytotoxic antibody could be found against HIV‐infected cells. Vice versa, sera of HIV‐1‐infected individuals did not exert a lytic effect in the presence of complement (of human or rabbit origin) against HIV‐1‐ or HTLV‐I‐infected cells. Incubation of the sera of four HTLV‐I‐infected patients with HTLV‐I env‐specific synthetic peptides demonstrated that some of the complement‐dependent cytotoxic antibodies recognized epitopes located on gp46 between amino acids 190 and 209. There is no correlation of rabbit complement‐dependent cytotoxic HTLV‐I antibodies with the development of disease.

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HIV-I and HIV-2 isolates differ in their ability to activate the complement system on the surface of infected cells

Cited by 34 publications

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Effect of Complement on HIV-2 Plasma Antiviral Activity Is Intratype Specific and Potent

Effect of Complement on HIV-2 Plasma Antiviral Activity Is Intratype Specific and Potent

Efficacy of HIV-specific and ‘antibody-independent’ mechanisms for complement activation by HIV-infected cells

Complement-dependent cytotoxic antibodies to human T lymphotropic virus type I (HTLV-I)-infected cells in the sera of HTLV-I-infected individuals

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