The COVID-19 pandemic and human fertility

Aassve, Arnstein; Cavalli, Nicolò; Mencarini, Letizia; Plach, Samuel; Bacci, Massimo Livi

doi:10.1126/science.abc9520

Cited by 176 publications

(127 citation statements)

References 14 publications

(18 reference statements)

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“…In a study analysing serum samples from hospitalized COVID-19 patients, antiphospholipid autoantibodies were detected in 52% of samples, which were further associated with neutrophil hyperactivity and more severe clinical outcomes [ 109 ]. Other studies have also identified autoantibodies against interferons, neutrophils, connective tissues, cyclic citrullinated peptides, and cell nucleus in 10–50% of patients with COVID-19 [ 110–112 , 113 ]. While it is unconfirmed if such autoantibodies are long-lasting in COVID-19, research review has strongly linked these autoantibodies to chronic autoimmune diseases, such as antiphospholipid and Sjogren syndromes, lupus erythematosus, and rheumatoid arthritis [ 114 ].…”

Section: Putative Pathophysiologymentioning

confidence: 99%

Long COVID or post-COVID-19 syndrome: putative pathophysiology, risk factors, and treatments

Yong

2021

Infectious Diseases

804

601

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Long COVID or post-COVID-19 syndrome first gained widespread recognition among social support groups and later in scientific and medical communities. This illness is poorly understood as it affects COVID-19 survivors at all levels of disease severity, even younger adults, children, and those not hospitalized. While the precise definition of long COVID may be lacking, the most common symptoms reported in many studies are fatigue and dyspnoea that last for months after acute COVID-19. Other persistent symptoms may include cognitive and mental impairments, chest and joint pains, palpitations, myalgia, smell and taste dysfunctions, cough, headache, and gastrointestinal and cardiac issues. Presently, there is limited literature discussing the possible pathophysiology, risk factors, and treatments in long COVID, which the current review aims to address. In brief, long COVID may be driven by long-term tissue damage (e.g. lung, brain, and heart) and pathological inflammation (e.g. from viral persistence, immune dysregulation, and autoimmunity). The associated risk factors may include female sex, more than five early symptoms, early dyspnoea, prior psychiatric disorders, and specific biomarkers (e.g. D-dimer, CRP, and lymphocyte count), although more research is required to substantiate such risk factors. While preliminary evidence suggests that personalized rehabilitation training may help certain long COVID cases, therapeutic drugs repurposed from other similar conditions, such as myalgic encephalomyelitis or chronic fatigue syndrome, postural orthostatic tachycardia syndrome, and mast cell activation syndrome, also hold potential. In sum, this review hopes to provide the current understanding of what is known about long COVID.

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Section: Putative Pathophysiologymentioning

confidence: 99%

Long COVID or post-COVID-19 syndrome: putative pathophysiology, risk factors, and treatments

Yong

2021

Infectious Diseases

804

601

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“…The XopQ/Roq1 complex ( Figure 12 c) shows that Roq1 recognizes XopQ by inserting a helical segment into the active site. Thus, Roq1 binds and blocks XopQ activity [ 93 ]. The right panel of Figure 12 c displays that the helical insertion of Roq1 superimposes with the XopQ helical lid in the closed conformation.…”

Section: The Importance Of α-Helical Domains In the (A) Virulence Of Bacterial Plant Pathogensmentioning

confidence: 99%

α-Helices in the Type III Secretion Effectors: A Prevalent Feature with Versatile Roles

Gazi

Kokkinidis

Fadouloglou

2021

IJMS

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Type III Secretion Systems (T3SSs) are multicomponent nanomachines located at the cell envelope of Gram-negative bacteria. Their main function is to transport bacterial proteins either extracellularly or directly into the eukaryotic host cell cytoplasm. Type III Secretion effectors (T3SEs), latest to be secreted T3S substrates, are destined to act at the eukaryotic host cell cytoplasm and occasionally at the nucleus, hijacking cellular processes through mimicking eukaryotic proteins. A broad range of functions is attributed to T3SEs, ranging from the manipulation of the host cell’s metabolism for the benefit of the bacterium to bypassing the host’s defense mechanisms. To perform this broad range of manipulations, T3SEs have evolved numerous novel folds that are compatible with some basic requirements: they should be able to easily unfold, pass through the narrow T3SS channel, and refold to an active form when on the other side. In this review, the various folds of T3SEs are presented with the emphasis placed on the functional and structural importance of α-helices and helical domains.

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“…Nevertheless, the first 15 years of experimental research with DNA vaccines failed to demonstrate Anti-Nuclear Autoantibody (ANA) positivity or autoimmune disease [ 59 ], with this rare complication being unmasked by mass vaccination programmes. Of note, the recognition of PF4-directed autoimmunity in VITT led to a search for the same autoantibody in severe COVID-19 pneumonia, where multiple autoantibodies -including anti-IFN and anti-endothelial cells autoantibodies-have been described [ [60] , [61] , [62] , [63] ]. Recently, autoantibodies directed against PF4 have been found in about 8% of COVID-19 cases but were of low magnitude compared to VITT and were not linked to immunothrombotic phenotypes [ 48 ], so are likely part of the known role of PF4- Anti -PF4 autoantibodies in natural immunity.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of Immunothrombosis in Vaccine-Induced Thrombotic Thrombocytopenia (VITT) Compared to Natural SARS-CoV-2 Infection

McGonagle

Marco

Bridgewood

2021

Journal of Autoimmunity

131

124

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Herein, we consider venous immunothrombotic mechanisms in SARS-CoV-2 infection and anti-SARS-CoV-2 DNA vaccination. Primary SARS-CoV-2 infection with systemic viral RNA release (RNAaemia) contributes to innate immune coagulation cascade activation, with both pulmonary and systemic immunothrombosis - including venous territory strokes. However, anti-SARS-CoV-2 adenoviral-vectored-DNA vaccines -initially shown for the ChAdOx1 vaccine-may rarely exhibit autoimmunity with autoantibodies to Platelet Factor-4 (PF4) that is termed Vaccine-Induced Thrombotic Thrombocytopenia (VITT), an entity pathophysiologically similar to Heparin-Induced Thrombocytopenia (HIT). The PF4 autoantigen is a polyanion molecule capable of independent interactions with negatively charged bacterial cellular wall, heparin and DNA molecules, thus linking intravascular innate immunity to both bacterial cell walls and pathogen-derived DNA. Crucially, negatively charged extracellular DNA is a powerful adjuvant that can break tolerance to positively charged nuclear histone proteins in many experimental autoimmunity settings, including SLE and scleroderma. Analogous to DNA-histone interactons, positively charged PF4-DNA complexes stimulate strong interferon responses via Toll-Like Receptor (TLR) 9 engagement. A chain of events following intramuscular adenoviral-vectored-DNA vaccine inoculation including microvascular damage; microbleeding and platelet activation with PF4 release, adenovirus cargo dispersement with DNA-PF4 engagement may rarely break immune tolerance, leading to rare PF4-directed autoimmunity. The VITT cavernous sinus cerebral and intestinal venous territory immunothrombosis proclivity may pertain to venous drainage of shared microbiotal-rich areas of the nose and in intestines that initiates local endovascular venous immunity by PF4/microbiotal engagement with PF4 autoantibody driven immunothrombosis reminiscent of HIT. According to the proposed model, any adenovirus-vectored-DNA vaccine could drive autoimmune VITT in susceptible individuals and alternative mechanism based on molecular mimicry, vaccine protein contaminants, adenovirus vector proteins, EDTA buffers or immunity against the viral spike protein are secondary factors. Hence, electrochemical DNA-PF4 interactions and PF4-heparin interactions, but at different locations, represent the common denominator in HIT and VITT related autoimmune-mediated thrombosis.

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The COVID-19 pandemic and human fertility

Abstract: Birth trends in response to the pandemic will vary according to socioeconomic conditions

Cited by 176 publications

References 14 publications

Long COVID or post-COVID-19 syndrome: putative pathophysiology, risk factors, and treatments

Long COVID or post-COVID-19 syndrome: putative pathophysiology, risk factors, and treatments

α-Helices in the Type III Secretion Effectors: A Prevalent Feature with Versatile Roles

Mechanisms of Immunothrombosis in Vaccine-Induced Thrombotic Thrombocytopenia (VITT) Compared to Natural SARS-CoV-2 Infection

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