Antibodies and infected monocytes and macrophages in COVID-19 patients

Darrell O. Ricke; Darrell O. Ricke

doi:10.3934/Allergy.2022007

AIMS Allergy and Immunology

2022, Volume 6, Issue 2: 64-70. doi: 10.3934/Allergy.2022007

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Letter Topical Sections

Antibodies and infected monocytes and macrophages in COVID-19 patients

Darrell O. Ricke ^,

Molecular BioInsights, Winchester, MA 01890, USA

Received: 28 May 2022 Accepted: 31 May 2022 Published: 08 June 2022

The SARS-CoV-2 virus causes the COVID-19 disease associated with over 6.2 million deaths globally. Multiple early indicators raised the potential risk of the SARS-CoV-2 virus infecting monocytes and macrophages via Fc-receptor antibody binding based on closely related beta coronaviruses. Antibody Fc-receptor infection of phagocytic monocytes and macrophages is one type of antibody dependent enhancement of disease. Increased COVID-19 severity correlated with early high antibody responses on initial infection for unvaccinated adults. Clinical evidence suggests that for moderate antibody titer levels, antibodies binding to SARS-CoV-2 may contribute to viral spread, cytokine dysregulation, and enhanced COVID-19 disease severity. Primary immune responses appear to have too low of antibody titer to significantly contribute to Fc-receptor uptake by monocytes and macrophages for COVID-19 patients. Very high antibody titers created by SARS-CoV-2 vaccines also appear to inhibit Fc-receptor uptake and infection of monocytes and macrophages; this inhibition appears to decrease as antibody titer levels decrease. Cross reactive antibodies to other coronaviruses or moderate levels of SARS-CoV-2 antibodies may be contributing to antibody dependent enhancement of disease in critical COVID-19 patients.
- antibodies,
- antibody dependent enhancement,
- ADE,
- COVID-19,
- monocytes,
- macrophages,
- vaccines
Citation: Darrell O. Ricke. Antibodies and infected monocytes and macrophages in COVID-19 patients[J]. AIMS Allergy and Immunology, 2022, 6(2): 64-70. doi: 10.3934/Allergy.2022007

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Abstract

The SARS-CoV-2 virus causes the COVID-19 disease associated with over 6.2 million deaths globally. Multiple early indicators raised the potential risk of the SARS-CoV-2 virus infecting monocytes and macrophages via Fc-receptor antibody binding based on closely related beta coronaviruses. Antibody Fc-receptor infection of phagocytic monocytes and macrophages is one type of antibody dependent enhancement of disease. Increased COVID-19 severity correlated with early high antibody responses on initial infection for unvaccinated adults. Clinical evidence suggests that for moderate antibody titer levels, antibodies binding to SARS-CoV-2 may contribute to viral spread, cytokine dysregulation, and enhanced COVID-19 disease severity. Primary immune responses appear to have too low of antibody titer to significantly contribute to Fc-receptor uptake by monocytes and macrophages for COVID-19 patients. Very high antibody titers created by SARS-CoV-2 vaccines also appear to inhibit Fc-receptor uptake and infection of monocytes and macrophages; this inhibition appears to decrease as antibody titer levels decrease. Cross reactive antibodies to other coronaviruses or moderate levels of SARS-CoV-2 antibodies may be contributing to antibody dependent enhancement of disease in critical COVID-19 patients.

Conflict of interest

The author declare no conflict of interest.

References

[1]	Ricke DO (2021) Two different antibody-dependent enhancement (ADE) risks for SARS-CoV-2 antibodies. Front Immunol 12: 443. https://doi.org/10.3389/fimmu.2021.640093
[2]	Jaume M, Yip MS, Cheung CY, et al. (2011) Anti-severe acute respiratory syndrome coronavirus spike antibodies trigger infection of human immune cells via a pH-and cysteine protease-independent FcγR pathway. J Virol 85: 10582-10597. https://doi.org/10.1128/JVI.00671-11
[3]	Junqueira C, Crespo Â, Ranjbar S, et al. (2022) FcγR-mediated SARS-CoV-2 infection of monocytes activates inflammation. Nature . In press. https://doi.org/10.1038/s41586-022-04702-4
[4]	Wan Y, Shang J, Sun S, et al. (2020) Molecular mechanism for antibody-dependent enhancement of coronavirus entry. J Virol 94: e02015-19. https://doi.org/10.1128/JVI.02015-19
[5]	Lee N, Chan PKS, Ip M, et al. (2006) Anti-SARS-CoV IgG response in relation to disease severity of severe acute respiratory syndrome. J Clin Virol 35: 179-184. https://doi.org/10.1016/j.jcv.2005.07.005
[6]	Peiris J, Lai S, Poon L, et al. (2003) Coronavirus as a possible cause of severe acute respiratory syndrome. Lancet 361: 1319-1325. https://doi.org/10.1016/S0140-6736(03)13077-2
[7]	Hsueh PR, Hsiao CH, Yeh SH, et al. (2003) Microbiologic characteristics, serologic responses, and clinical manifestations in severe acute respiratory syndrome, Taiwan. Emerg Infect Dis 9: 1163-1167. https://doi.org/10.3201/eid0909.030367
[8]	Wang H, Rao S, Jiang C (2007) Molecular pathogenesis of severe acute respiratory syndrome. Microbes Infect 9: 119-126. https://doi.org/10.1016/j.micinf.2006.06.012
[9]	Pujadas E, Chaudhry F, McBride R, et al. (2020) SARS-CoV-2 viral load predicts COVID-19 mortality. Lancet Respir Med 8: e70. https://doi.org/10.1016/S2213-2600(20)30354-4
[10]	Yan X, Chen G, Jin Z, et al. (2022) Anti-SARS-CoV-2 IgG levels in relation to disease severity of COVID-19. J Med Virol 94: 380-383. https://doi.org/10.1002/jmv.27274
[11]	Luo YR, Chakraborty I, Yun C, et al. (2021) Kinetics of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) antibody avidity maturation and association with disease severity. Clin Infect Dis 73: e3095-e3097. https://doi.org/10.1093/cid/ciaa1389
[12]	Fajnzylber J, Regan J, Coxen K, et al. (2020) SARS-CoV-2 viral load is associated with increased disease severity and mortality. Nat Commun 11: 5493. https://doi.org/10.1038/s41467-020-19057-5
[13]	Chen W, Zhang J, Qin X, et al. (2020) SARS-CoV-2 neutralizing antibody levels are correlated with severity of COVID-19 pneumonia. Biomed Pharmacother 130: 110629. https://doi.org/10.1016/j.biopha.2020.110629
[14]	Chen H, Qin R, Huang Z, et al. (2021) Characteristics of COVID-19 patients based on the results of nucleic acid and specific antibodies and the clinical relevance of antibody levels. Front Mol Biosci 7: 605862. https://doi.org/10.3389/fmolb.2020.605862
[15]	Young BE, Ong SWX, Ng LFP, et al. (2021) Viral dynamics and immune correlates of coronavirus disease 2019 (COVID-19) severity. Clin Infect Dis 73: e2932-e2942. https://doi.org/10.1093/cid/ciaa1280
[16]	Liu X, Wang J, Xu X, et al. (2020) Patterns of IgG and IgM antibody response in COVID-19 patients. Emerg Microbes Infect 9: 1269-1274. https://doi.org/10.1080/22221751.2020.1773324
[17]	Atyeo C, Fischinger S, Zohar T, et al. (2020) Distinct early serological signatures track with SARS-CoV-2 survival. Immunity 53: 524-532. https://doi.org/10.1016/j.immuni.2020.07.020
[18]	Fraley E, LeMaster C, Banerjee D, et al. (2021) Cross-reactive antibody immunity against SARS-CoV-2 in children and adults. Cell Mol Immunol 18: 1826-1828. https://doi.org/10.1038/s41423-021-00700-0
[19]	Shrwani K, Sharma R, Krishnan M, et al. (2021) Detection of serum cross-reactive antibodies and memory response to SARS-CoV-2 in prepandemic and post-COVID-19 convalescent samples. J Infect Dis 224: 1305-1315. https://doi.org/10.1093/infdis/jiab333
[20]	Miyara M, Saichi M, Sterlin D, et al. (2022) Pre-COVID-19 immunity to common cold human coronaviruses induces a recall-type IgG response to SARS-CoV-2 antigens without cross-neutralisation. Front Immunol 13: 790334. https://doi.org/10.3389/fimmu.2022.790334
[21]	Aguilar-Bretones M, Westerhuis BM, Raadsen MP, et al. (2021) Seasonal coronavirus-specific B cells with limited SARS-CoV-2 cross-reactivity dominate the IgG response in severe COVID-19. J Clin Invest 131: e150613. https://doi.org/10.1172/JCI150613
[22]	Cheng Y, Wong R, Soo YOY, et al. (2005) Use of convalescent plasma therapy in SARS patients in Hong Kong. Eur J Clin Microbiol 24: 44-46. https://doi.org/10.1007/s10096-004-1271-9
[23]	Korley FK, Durkalski-Mauldin V, Yeatts SD, et al. (2021) Early convalescent plasma for high-risk outpatients with Covid-19. N Engl J Med 385: 1951-1960. https://doi.org/10.1056/NEJMoa2103784
[24]	Horby PW, Landray MJ, Grp RC (2021) Convalescent plasma in patients admitted to hospital with COVID-19 (RECOVERY): a randomised controlled, open-label, platform trial. Lancet 397: 2049-2059. https://doi.org/10.1016/S0140-6736(21)00897-7
[25]	De Santis GC, Oliveira LC, Garibaldi PMM, et al. (2022) High-dose convalescent plasma for treatment of severe COVID-19. Emerg Infect Dis 28: 548-555. https://doi.org/10.3201/eid2803.212299
[26]	Axfors C, Janiaud P, Schmitt AM, et al. (2021) Association between convalescent plasma treatment and mortality in COVID-19: a collaborative systematic review and meta-analysis of randomized clinical trials. BMC Infect Dis 21: 1170. https://doi.org/10.1186/s12879-021-06829-7
[27]	García-Nicolás O, V'kovski P, Zettl F, et al. (2021) No evidence for human monocyte-derived macrophage infection and antibody-mediated enhancement of SARS-CoV-2 infection. Front Cell Infect Microbiol 11: 644574. https://doi.org/10.3389/fcimb.2021.644574
[28]	Boumaza A, Gay L, Mezouar S, et al. (2021) Monocytes and macrophages, targets of severe acute respiratory syndrome coronavirus 2: the clue for coronavirus disease 2019 immunoparalysis. J Infect Dis 224: 395-406. https://doi.org/10.1093/infdis/jiab044
[29]	Martines RB, Ritter JM, Matkovic E, et al. (2020) Pathology and pathogenesis of SARS-CoV-2 associated with fatal coronavirus disease, United States. Emerg Infect Dis 26: 2005-2015. https://doi.org/10.3201/eid2609.202095
[30]	Grant RA, Morales-Nebreda L, Markov NS, et al. (2021) Circuits between infected macrophages and T cells in SARS-CoV-2 pneumonia. Nature 590: 635-641. https://doi.org/10.1038/s41586-020-03148-w
[31]	Feng Z, Diao B, Wang R, et al. (2020) The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) directly decimates human spleens and lymph nodes. medRxiv Preprint . https://doi.org/10.1101/2020.03.27.20045427
[32]	Wang C, Xie J, Zhao L, et al. (2020) Alveolar macrophage dysfunction and cytokine storm in the pathogenesis of two severe COVID-19 patients. eBioMedicine 57: 102833. https://doi.org/10.1016/j.ebiom.2020.102833
[33]	Martínez-Colón GJ, Ratnasiri K, Chen H, et al. (2021) SARS-CoV-2 infects human adipose tissue and elicits an inflammatory response consistent with severe COVID-19. bioRxiv Preprint . https://doi.org/10.1101/2021.10.24.465626
[34]	Tavazzi G, Pellegrini C, Maurelli M, et al. (2020) Myocardial localization of coronavirus in COVID-19 cardiogenic shock. Eur J Heart Fail 22: 911-915. https://doi.org/10.1002/ejhf.1828
[35]	Yang L, Han Y, Jaffré F, et al. (2021) An immuno-cardiac model for macrophage-mediated inflammation in COVID-19 hearts. Circ Res 129: 33-46. https://doi.org/10.1161/CIRCRESAHA.121.319060
[36]	Percivalle E, Sammartino JC, Cassaniti I, et al. (2021) Macrophages and monocytes: “Trojan horses” in COVID-19. Viruses 13: 2178. https://doi.org/10.3390/v13112178

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