ReviewInternational archives of allergy and immunology2022
The Contribution of Complement Protein C1q in COVID-19 and HIV Infection Comorbid with Preeclampsia: A Review.
Review in International archives of allergy and immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Enhancing decision-making with linear diophantine multi-fuzzy set: application of novel information measures in medical and engineering fields.Scientific reports · 2024Article
- Differential expression of the angiotensin receptors (AT1, AT2, and AT4) in the placental bed of HIV-infected preeclamptic women of African ancestry.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Article
- Molecular Biomarker Identification Using a Network-Based Bioinformatics Approach That Links COVID-19 With Smoking.Bioinformatics and biology insights · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulation in component 1q (C1q) levels is associated with weak placental development in preeclampsia (PE). Human immunodeficiency virus infection (HIV-1) triggers the C1q complex, resulting in opsonization of healthy host cells, contributing to their removal, and augmented progression of HIV disease. In coronavirus disease 2019 (COVID-19)-infected patients, the deposition of C1q activates the complement. Considering the paucity of data, this review highlights a significant gap in the potential of C1q in the immunocompromised state of preeclamptic HIV-infected women and COVID-19 infection. In PE, C1q is downregulated; while in antiretroviral treatment-treated HIV/COVID-19 infected patients, C1q is upregulated. It is plausible that C1q is augmented in the triad and may exacerbate severity of disease. This thereby provides a foundation for future intended research which involves the investigation of single nucleotide polymorphism expression of the C1q gene, specifically in these diseases.
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Registered trials
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