The lectin pathway of complement: Advantage or disadvantage in HIV pathogenesis?

Ballegaard, Vibe; Haugaard, Anna Karen; Garred, Peter; Nielsen, Susanne Dam; Munthe-Fog, Lea

doi:10.1016/j.clim.2014.06.002

Cited by 15 publications

(14 citation statements)

References 127 publications

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“…Early after infection, complement is activated through the classical pathway in combination with anti‐envelope and neutralizing antibodies to mediate viral lysis . In addition, C1q and mannose binding protein directly bind the HIV surface proteins gp41 and gp120, leading to complement activation without antibodies . Complement‐mediated neutralization of HIV participates in host immune responses throughout the course of infection, but is not sufficiently effective to control or eliminate it.…”

Section: Discussionmentioning

confidence: 99%

Plasma levels of soluble membrane attack complex are elevated despite viral suppression in HIV patients with poor immune reconstitution

Schein

Blackburn

Heath

et al. 2019

Clinical and Experimental Immunology

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The complement system is now a therapeutic target for the management of serious and life-threatening conditions such as paroxysmal nocturnal hemoglobinuria, atypical hemolytic uremic syndrome, glomerulonephritis and other diseases caused by complement deficiencies or genetic variants. As complement therapeutics expand into more clinical conditions, monitoring complement activation is increasingly important, as is the baseline levels of complement activation fragments in blood or other body fluid levels. Although baseline complement levels have been reported in the literature, the majority of these data were generated using non-standard assays and with variable sample handling, potentially skewing results. In this study, we examined the plasma and serum levels of the soluble membrane attack complex of complement (sMAC). sMAC is formed in the fluid phase when complement is activated through the terminal pathway. It binds the regulatory proteins vitronectin and/or clusterin and cannot insert into cell membranes, and can serve as a soluble diagnostic marker in infectious disease settings, as previously shown for intraventricular shunt infections. Here we show that in healthy adults, serum sMAC levels were significantly higher than those in plasma, that plasma sMAC levels were similar between in African Americans and Caucasians and that plasma sMAC levels increase with age. Plasma sMAC levels were significantly higher in virally suppressed people living with HIV (PLWH) compared to non-HIV infected healthy donors. More specifically, PLWH with CD4 + T cell counts below 200 had even greater sMAC levels, suggesting diagnostic value in monitoring sMAC levels in this group.

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Section: Discussionmentioning

confidence: 99%

Plasma levels of soluble membrane attack complex are elevated despite viral suppression in HIV patients with poor immune reconstitution

Schein

Blackburn

Heath

et al. 2019

Clinical and Experimental Immunology

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“…39). One of these lectins, the mannose-binding lectin (MBL), plays an important part in innate immunity by binding carbohydrates on the surface of many pathogens 40 and activating the complement system. For example, lower MBL levels are associated with susceptibility to Streptococcus pneumoniae, Neisseria meningitidis and influenza A virus, as well as with the severity of hepatitis B infection (reviewed in REF.…”

Section: Transmission Bottlenecks In the Donormentioning

confidence: 99%

Bottlenecks in HIV-1 transmission: insights from the study of founder viruses

et al. 2015

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HIV-1 infection typically results from the transmission of a single viral variant, the transmitted/founder (T/F) virus. Studies of these HIV-1 variants provide critical information about the transmission bottlenecks and the selective pressures acting on the virus in the transmission fluid and in the recipient tissues. These studies reveal that T/F virus phenotypes are shaped by stochastic and selective forces that restrict transmission and may be targets for prevention strategies. In this Review, we highlight how studies of T/F viruses contribute to a better understanding of the biology of HIV-1 transmission and discuss how these findings affect HIV-1 prevention strategies.

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“…Since AV reportedly does not bind to WSSV directly (Luo et al, 2003), and we predict that it contains a signal peptide, we postulate that AV is involved in a signal pathway or protein complex that functions in extracellular shrimp immunity. Mannose-binding lectins have recently been reported to perform dual functions in defending against disease (Ibernon et al, 2014) and the complement system, of which mannose-binding lectin is a component, may be a double-edged sword during human immunodeficiency virus infection (Ballegaard et al, 2014). While our data indicate that AV may delay propagation of WSSV in both L. vannamei and P. monodon (Pathan et al, 2013), the underlying molecular mechanisms remain unclear.…”

Section: Discussionmentioning

confidence: 74%

Molecular characterization of LvAV in response to white spot syndrome virus infection in the Pacific white shrimp (Litopenaeus vannamei)

Song²,

Qian

et al. 2015

Developmental & Comparative Immunology

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The lectin pathway of complement: Advantage or disadvantage in HIV pathogenesis?

Cited by 15 publications

References 127 publications

Plasma levels of soluble membrane attack complex are elevated despite viral suppression in HIV patients with poor immune reconstitution

Plasma levels of soluble membrane attack complex are elevated despite viral suppression in HIV patients with poor immune reconstitution

Bottlenecks in HIV-1 transmission: insights from the study of founder viruses

Molecular characterization of LvAV in response to white spot syndrome virus infection in the Pacific white shrimp (Litopenaeus vannamei)

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