Two parallel routes of the complement-mediated antibody-dependent enhancement of HIV-1 infection

Prohászka, Zoltán; Nemes, Judit; Hidvegi, Tunda; Tóth, Ferenc; Kerekes, Krisztina; Erdei, Anna; Szabó, Judit; Újhelyi, Eszter; Thielens, Nicole M.; Dierich, Manfred P.; Späth, Peter; Ghebrehiwet, Berhane; Hampl, H.; Kiss, J.; Arlaud, Gérard J.; Füst, George

doi:10.1097/00002030-199708000-00002

Cited by 41 publications

(31 citation statements)

References 26 publications

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“…Another mechanism could involve complement-mediated, antibody-dependent enhancement of HIV-1 infection. HIV-IgA immune complexes could be coated by C3 fragments; the interaction between virusbound C3 and CR2 (CD21) has been reported elsewhere to enhance HIV-1 infection [24].…”

Section: Discussionmentioning

confidence: 85%

Neutralization of Human Immunodeficiency Virus Type 1 (HIV‐1) Mediated by Parotid IgA of HIV‐1–Infected Patients

Moja¹,

Tranchat²,

Tchou³

et al. 2000

J INFECT DIS

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Infection with human immunodeficiency virus type 1 (HIV-1) has been shown to elicit a serum antibody response with neutralizing activity against T cell line-adapted HIV strains and primary HIV-1 isolates. Mucosal surfaces are the primary route of HIV-1 infection. Evidence is presented here for the presence of HIV-neutralizing antibodies in secretions. Infection of mucosal cells with HIV stimulates systemic and mucosal immune responses and results in the generation of neutralizing antibodies. Serum IgG and IgA neutralize HIV-1MN infection of susceptible T cell lines; serum IgG inhibits more effectively. Mucosal IgA purified from parotid saliva of HIV-1-seropositive individuals could neutralize both a T cell line-adapted strain and a primary isolate. The neutralizing activity of IgA was not directed against the anti-third-variable-loop or the anti-ELDKWA epitope. Thus, the specificity of mucosal IgA for HIV-1 neutralization epitopes remains to be determined and may provide insight into development of a mucosal vaccine.

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Section: Discussionmentioning

confidence: 85%

Neutralization of Human Immunodeficiency Virus Type 1 (HIV‐1) Mediated by Parotid IgA of HIV‐1–Infected Patients

Moja¹,

Tranchat²,

Tchou³

et al. 2000

J INFECT DIS

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“…Indeed, viruses from various families elicit antibodies that enhance infectivity through the binding of virus-antibody complexes to cellular Fc receptors (expressed in, e.g., monocytes/macrophages) via the Fc portion of the antibodies (24,44,49). Fixation of the C3 or C1q complement proteins, activated by virus-antibody complexes, can also facilitate virus entry, as shown for the antibody-dependent, complement-mediated enhancement of infection of human immunodeficiency virus (19,46,53) and Ebola virus (54). Finally, in vitro enhancement of human immunodeficiency virus infection via an antibody-independent mechanism that involves receptors of the classical and alternative complement pathways has been reported (5,21).…”

Section: Discussionmentioning

confidence: 99%

Human Serum Facilitates Hepatitis C Virus Infection, and Neutralizing Responses Inversely Correlate with Viral Replication Kinetics at the Acute Phase of Hepatitis C Virus Infection

Lavillette

Morice

Germanidis³

et al. 2005

J Virol

250

202

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The factors leading to spontaneous clearance of hepatitis C virus (HCV) or to viral persistence are elusive. Understanding virus-host interactions that enable acute HCV clearance is key to the development of more effective therapeutic and prophylactic strategies. Here, using a sensitive neutralization assay based on infectious HCV pseudoparticles (HCVpp), we have studied the kinetics of humoral responses in a cohort of acute-phase patients infected during a single nosocomial outbreak in a hemodialysis center. The 17 patients were monitored for the spontaneous outcome of HCV infection for 6 months before a treatment decision was made. Blood samples were taken frequently (15 ؎ 4 per patient). Phylogenetic analysis of the predominant virus(es) revealed infection by only one of two genotype 1b strains. While all patients seroconverted, their sera induced two opposing effects in HCVpp infection assays: inhibition and facilitation. Furthermore, the ability of sera to facilitate or inhibit infection correlated with the presence of either infecting HCV strain and divided the patients into two groups. In group 1, the progressive emergence of a relatively strong neutralizing response correlated with a fluctuating decrease in high initial viremia, leading to control of viral replication. Patients in group 2 failed to reduce viremia within the acute phase, and no neutralizing responses were detected despite seroconversion. Strikingly, sera of group 2, as well as naïve sera, facilitated infection by HCVpp displaying HCV glycoproteins from different genotypes and strains, including those retrieved from patients. These results provide new insights into the mechanisms of viral persistence and immune control of viremia.Hepatitis C virus (HCV) infection causes acute hepatitis after 4 to 12 weeks of incubation. Acute hepatitis is characterized by elevated alanine aminotransferase (ALT) levels, with generally no or only mild symptoms. Among infected individuals, only 20% clear infection spontaneously, whereas ϳ80% progress to chronic infection. Chronic hepatitis may lead after 10 to 30 years to severe, life-threatening complications, such as cirrhosis and hepatocellular carcinoma. With an estimated 170 million people infected, i.e., nearly 3% of the world population, and an incidence of ϳ3 to 4 million new infections per year, HCV is presently a leading cause of chronic liver disease and poses a major public health problem. In the United States, HCV constitutes the most common chronic blood-borne infectious disease and is the principal indication for liver transplantation and the 10th leading cause of deaths among adults. The only approved therapy for chronic hepatitis C is the combination of alpha interferon, used in a pegylated form, and ribavirin. This treatment cures infection in a significant proportion of patients, but its efficacy against HCV genotype 1, the most frequent HCV genotype in industrialized countries, remains limited, and it can cause significant side effects (18,23,36). HCV is a highly variable virus that compri...

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“…The resultant complex, consisting of the virus, antibodies and C1q, binds C1q receptors (C1qR) at the cell surface, promoting either binding of the virus to Ebola virus-specific receptors or endocytosis of the target cells by intracellular signalling via C1qR [69,70]. Prohaszka et al [71] also suggested that C1q-mediated ADE might underlie HIV infection, although the mechanism of enhancement remains elusive, since C1q directly binds to HIV gp41 [69,72].…”

Section: Ebola Virusmentioning

confidence: 99%

Antibody‐dependent enhancement of viral infection: molecular mechanisms and in vivo implications

Takada¹,

Kawaoka²

2003

Reviews in Medical Virology

297

247

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Besides the common receptor/coreceptor-dependent mechanism of cellular attachment, some viruses rely on antiviral antibodies for their efficient entry into target cells. This mechanism, known as antibody-dependent enhancement (ADE) of viral infection, depends on the cross-linking of complexes of virus-antibody or virus-activated complement components through interaction with cellular molecules such as Fc receptors or complement receptors, leading to enhanced infection of susceptible cells. Recent studies have suggested that additional mechanisms underlie ADE: involvement of complement component C1q and its receptor (Ebola virus), antibody-mediated modulation of the interaction between viral protein and its coreceptor (human immunodeficiency virus) and suppression of cellular antiviral genes by the replication of viruses entering cells via ADE (Ross River virus). Since ADE is exploited by a variety of viruses and has been associated with disease exacerbation, it may have broad relevance to the pathogenesis of viral infection and antiviral strategies.

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Two parallel routes of the complement-mediated antibody-dependent enhancement of HIV-1 infection

Cited by 41 publications

References 26 publications

Neutralization of Human Immunodeficiency Virus Type 1 (HIV‐1) Mediated by Parotid IgA of HIV‐1–Infected Patients

Neutralization of Human Immunodeficiency Virus Type 1 (HIV‐1) Mediated by Parotid IgA of HIV‐1–Infected Patients

Human Serum Facilitates Hepatitis C Virus Infection, and Neutralizing Responses Inversely Correlate with Viral Replication Kinetics at the Acute Phase of Hepatitis C Virus Infection

Antibody‐dependent enhancement of viral infection: molecular mechanisms and in vivo implications

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