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Case Study

Explaining the unexpected COVID-19 trends and potential impact across Africa.

[version 1; peer review: 1 approved with reservations]
Daniel Oduro-Mensah
https://orcid.org/0000-0003-4492-2202
1,2, Ebenezer Oduro-Mensah3, Peter Quashie2,4, Gordon Awandare1,2, Laud Okine1,2
Daniel Oduro-Mensah
https://orcid.org/0000-0003-4492-2202
1,2, Ebenezer Oduro-Mensah3, [...] Peter Quashie2,4, Gordon Awandare1,2, Laud Okine1,2
PUBLISHED 22 Nov 2021
Author details Author details
OPEN PEER REVIEW
REVIEWER STATUS

This article is included in the Emerging Diseases and Outbreaks gateway.

Abstract

Official COVID-19 case counts and mortality rates across Africa are lower than had been anticipated. Research reports, however, indicate far higher exposure rates than the official counts in some countries. Particularly in Western and Central Africa, where mortality rates are disproportionately lower than the rest of the continent, this occurrence may be due to immune response adaptations resulting from (1) frequent exposure to certain pro-inflammatory pathogens, and (2) a prevalence of low-grade inflammation coupled with peculiar modifications to the immune response based on one’s immunobiography. We suggest that the two factors lead to a situation where post infection, there is a rapid ramp-up of innate immune responses, enough to induce effective defense and protection against plethora pathogens. Alongside current efforts at procuring and distributing vaccines, we draw attention to the need for work towards appreciating the impact of the apparently widespread, asymptomatic SARS-CoV-2 infections on Africa’s populations vis a vis systemic inflammation status and long-term consequences for public health.

Keywords

COVID-19, Immunobiography, Inflamm-aging, Inflammation, Long COVID

Corresponding author: Daniel Oduro-Mensah
Competing interests: No competing interests were disclosed.
Grant information: The author(s) declared that no grants were involved in supporting this work.
Copyright:  © 2021 Oduro-Mensah D et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
How to cite: Oduro-Mensah D, Oduro-Mensah E, Quashie P et al. Explaining the unexpected COVID-19 trends and potential impact across Africa. [version 1; peer review: 1 approved with reservations]. F1000Research 2021, 10:1177 (https://doi.org/10.12688/f1000research.74363.1) First published: 22 Nov 2021, 10:1177 (https://doi.org/10.12688/f1000research.74363.1) Latest published: 21 Nov 2022, 10:1177 (https://doi.org/10.12688/f1000research.74363.2)

List of abbreviations

COVID: coronavirus disease

LGI: low-grade inflammation

PASC: post-acute sequelae of COVID-19

SARS-CoV-2: severe acute respiratory syndrome coronavirus 2

Introduction

Despite predictions of being among the worst affected globally, the trajectory of COVID-19 in Africa has been radically different, with far lower morbidity and mortality figures than recorded in the United Kingdom, India, Brazil, the Americas, and across Europe.1 By July 2021, Africa contributed approximately 2 % of global COVID-19 case reports.2 Considering Africa’s relatively ill-resourced healthcare settings, mainly across sub-Saharan Africa, it seems to follow that COVID-19 patients who require hospital admission are disproportionately more likely to die.3 However, Africa’s 16.72 % share of the global population4 contributed only up to 3.5 % of global COVID-19 mortality by July 2021.1,5 From December 2020 when emerging SARS-CoV-2 variants fueled second and third waves of COVID-19 across the globe6–11 from December 2020, Africa’s case reports declined steadily from January to mid-May 2021, climbed up sharply and started another decline at the end of June 2021.1,12–14 Interestingly among Africa’s five regions, countries in Western and Central Africa appear to be least affected by the COVID-19 pandemic (Figure 1).15 As of September 2021, the two regions which make up 43.5 % of Africa’s 1.4 billion population16 contributed only 13 % of Africa’s COVID-19 morbidity and 8 % of mortality figures.

05b37a34-3129-48e1-a921-53385587f2ef_figure1.gif

Figure 1. Overlap between COVID-19-related mortality and occurrence of malaria across Africa.

Sources: https://www.statista.com/, https://covid19.who.int/; Accessed September 8, 2021.

Attempts at explaining Africa’s trends include suggestions that not enough testing has been done in the region,17,18 that Africa has a relatively young population,19,20 the systematic use of antimalarials in parts of Africa21 and that the third-world conditions across most of the region may mean that people have previously been exposed to viruses molecularly similar to SARS-CoV-2.22–25 Others have suggested that exposure to similarly inflammatory conditions/pathogens may have led to a situation where individuals have adapted to the effects of inflammation and so are less sensitive to the SARS-CoV-2-induced inflammatory events which are the main drivers of COVID-19 pathogenesis.26–29 Here,1 we discuss evidence in support of the modification of the immune response due to frequent exposure to inflammatory pathogens, citing malaria, and2 present a second reason to explain why most parts of Africa have been relatively spared the worst of COVID-19.

Frequent exposure to malaria

Approximately 85 % of global malaria incidence is in Africa.30 Of Africa’s five regions, Western and Central Africa are reported to have the highest malaria incidence, contributing up to 71 % of Africa’s total. In 2017, an inverse relationship between the pro-inflammatory response and exposure to malaria was reported.31 Contrastingly, naïve individuals exhibited a more pro-inflammatory response with higher circulating levels of pro-inflammatory immune mediators.32,33 Individuals residing in malaria endemic zones often harbor Plasmodium spp. infections but are clinically immune.34,35 Pro-inflammatory mediators are important in expressing the clinical presentation of malaria. It has been suggested that repeated episodes of febrile malaria alter the immune response, resulting in a blunted inflammatory response which shows low levels of pro-inflammatory cytokines and appears to be dominated by anti-inflammatory cytokines.36 This likely plays a significant role in the apparent immunologic tolerance manifesting as clinical immunity to malaria.34,35,37 In addition, there appears to be upregulation of certain components of the innate immune response, including phagocytes and interferon-gamma, in frequently exposed individuals.36,38,39 We suggest that this altered immune response, characterized by low pro-inflammatory mediator levels, high anti-inflammatory mediator levels and up-regulated innate immune components, offers some protection against SARS-CoV-2-induced inflammation.

In individuals with the altered response due to frequent malaria exposure, SARS-CoV-2 infection may be met by a heightened innate response which overwhelms the reported blocking of some innate immune response pathways by the virus.40–44 Our submission, therefore, is that although this heightened innate response is limiting to the virus, it does not elicit enough of a pro-inflammatory adaptive response which could lead to the classical COVID-19-associated hyperinflammation. Consequently, the result of SARS-CoV-2-induced inflammation is not the cytokine ‘storm’ that occurs in severe COVID-19, but a milder cytokine ‘drizzle’ that minimizes the deleterious effects of the inflammatory response. This is contrary suggestions, including that by Kusi et al.,27 that the innate response may be negatively associated with the observed immunopathology of COVID-19. We maintain that viral load would effectively be suppressed by the innate response, consistent with suggestions by Stertz and Hale,43 with a slow ramp-up in inflammatory cytokine production due to the blunted pro-inflammatory adaptive response. Therefore, patients would only experience mild COVID-19 symptoms, or even have asymptomatic infections. A study on patients in China with asymptomatic COVID-19 revealed that they had relatively lower levels of serum alanine aminotransferase (ALA) and C-reactive protein.45 Previously, it has been shown that ALA may correlate negatively with T cell and natural killer cell activity.46 This supports the suggestion that in individuals with asymptomatic infection, there may be a sharper cell-mediated innate response which significantly moderates the progression to a pro-inflammatory, adaptive immune response.

It is striking how patterns of malaria endemicity appear to contrast COVID-19 mortality patterns in several places across Africa. Countries with the least malaria are the most affected by COVID-related mortality (Figure 1). Only one (Nigeria) of the top ten malaria endemic countries in Africa was in the top ten of country reports on Africa’s COVID-19 mortality rates as of September 2021. This is likely to be because Nigeria has Africa’s largest population by far. Outside Africa, using Brazil as an example, only one of the top ten malaria endemic areas, Goias, was in the country’s top ten COVID-19 mortality count, at 8th place as of September 2021.47,48 Meanwhile, Brazil was the world’s second most affected country by COVID-19 mortality at the time.49

In addition to Plasmodium spp., other pro-inflammatory pathogens including helminths and human coronaviruses as may be common and/or endemic in many parts of Africa could potentially have similar effects.27,50–52 It is unclear, however, whether their effects may be as protective as the malaria effect we allude to. Human coronaviruses (HCoV), for example, has been suggested to play a role in the apparent protection from SARS-CoV-2 due to observed cross-reactivity between HCoV-exposd sera and SARS-CoV-2 antigen.25,53 However, a contrasting observation suggests that pre-exposure to certain HCoV variants correlates positively with severity of COVID-19.54

Low-grade inflammation

Low-grade inflammation (LGI) is a state of persistent, low level systemic inflammation marked by approximately 2–4-fold increases in circulating immune pro-inflammatory markers.55–58 LGI may be due to chronic exposure to stimulatory environmental and lifestyle factors including stress, asymptomatic infections, bad oral hygiene practices, bad diet, obesity, traumatic injury, sedentary behavior, and smoke inhalation.59–61 The third world living conditions across much of Africa have long fueled a suspicion that LGI might be a relatively widespread phenomenon. Recently, this suspicion has been backed by the increasing reports of full-blown chronic inflammatory diseases among Africa’s populations.62,63 In individuals with LGI, changes in the immune response may include (1) reduced macrophage function, (2) decreased cytokine production in response to immune challenge, (3) decreased number of naïve T and B cells, (4) altered toll-like receptor expression and signaling, and (5) diminished response to antigen or mitogen stimulation.64 These changes suggest that both the innate and adaptive pro-inflammatory response would be at lower levels relative to individuals without LGI.

At the start of the pandemic, it was predicted that individuals with underlying chronic disease conditions that have systemic inflammation as a common feature would be prone to more severe forms of COVID-19.65–67 The expectation was that due to the pre-existing immune inflammatory dysfunction, the inflammatory response of such individuals would quickly spiral into hyperinflammation in response to SARS-CoV-2 infection. The situation would be similar for people with low grade inflammation or inflamm-aging but who did not yet have full-blown chronic diseases.68–70 This, however, appears not to have been the case. Looking at obesity for example, which is a model for LGI, a recent study on patients in America reported that in the first few days after diagnosis, levels of selected inflammation markers were lower in obese COVID-19 patients than in non-obese patients.71 Previous studies on influenza had reported that obese individuals (with LGI) mounted a slow pro-inflammatory response to the respiratory virus, with impaired pathogen-induced and lung-specific responses.72,73 This impaired adaptive pro-inflammatory response was suggested to contribute to the worse COVID-19 clinical outcomes in obese patients.74–76 In contrast, we suggest that the delayed response is rather protective, much like in the case of malaria exposure previously described. The worse COVID-19 outcomes in obese patients are more likely found in those with underlying chronic inflammatory diseases77–80 and are probably due to a combination of factors including extensive dysfunction and dysregulation of the inflammatory response.71,81–84 We suggest that, after an inflammatory response is mounted, appropriate metabolic regulation of the response is easily overwhelmed in patients with LGI-related comorbidities. In individuals with only LGI, however, the dysfunction is present but is not so extensive as to have caused organ damage and subsequent chronic disease. Relative to other persons, the already higher circulating levels of inflammatory mediators in LGI individuals feed an immune response, but escalation of the response is impaired. Therefore, there is a slow ramp-up of the pro-inflammatory response coupled with appreciable inflammatory response regulation, a combination which tends to be protective against COVID-19 progression.

Our suggestion is backed by the observation that with the start of vaccination against COVID-19, literature from outside Africa suggest that older adults are less likely to report adverse effects after vaccination.85–87 Our interpretation of this is that the phenomenon of inflamm-aging, which has characteristics similar to low grade inflammation,58,88–91 appears to protect against vaccine side effects. This implies that the combination of higher systemic levels of inflammatory mediators, a blunt pro-inflammatory adaptive immune response, and an apparently impaired innate immune response are useful against COVID-19. In the African population, however, our thinking is that the innate response is not impaired. Rather, as described in the previous section, the history of frequent exposure to pro-inflammatory pathogens leaves the innate response at a higher level relative to individuals from other populations. This may explain why even older Africans appear to have better protection from the virus than older adults from elsewhere. This imprint of immune history on the specific modifications to an individual’s immune response would be consistent with the concept of immunobiography,58,92 which suggests close links between human health, longevity and individual immune system modifications.58,92–95

Outlook

The focus on COVID-19 characterization and management had been on the clinical presentation of acutely ill patients. Only approximately 14 % of COVID-19 cases are severe enough to require hospital admission.96 References to the 86 % majority who experienced only mild/moderate or asymptomatic COVID-19 usually had to do with the tracking of the infection rate and transmission dynamics. Given the indications that an individual’s systemic inflammation state is altered post SARS CoV-2 infection, there had been the suspicion that even people with asymptomatic infection or mild COVID-19 symptoms would experience some sort of post-acute syndrome. Reports from across the world have indicated such a situation, showing that up to 50 % of non-hospitalized patients who experience mild or moderate COVID-19 continue to have symptoms up to six months and beyond after recovery.97–100 This has since been termed post-acute sequelae of COVID-19 (PASC). Health issues associated with PASC include fatigue, exercise intolerance, cognitive impairment, anxiety/depression, organ damage, impaired mobility, and reduced quality of life,101–104 all of which are also associated with LGI and inflamm-aging.58,105

The prevailing social and environmental conditions across Africa likely mean that the spread of SARS-CoV-2 has been rather extensive. This is supported, for example, by the observation of a 13–27 % average seroprevalence of SARS-CoV-2 antibodies in randomly sampled individuals across Ghana,106 compared to official figures of approximately 0.41 % for cumulative total infection rate as of September 2021.107 Similar situations have been reported in other African countries.108,109 Interestingly, the 60+ age group showed the highest seropositivity rate 106. Keeping in mind that the antibody test kit used had shown up to 66 % sensitivity and at least 94 % specificity,106 the report suggested that the observation of low sensitivity of antibody test kits may be due to generally low production of antibodies by infected persons rather than a failure of the kits used. The low sensitivity is interesting, particularly when some studies report significant cross-reactivity between other human coronaviruses antibodies and SARS-CoV-2 antigens.25 The likely underestimation of seropositivity106 suggests that far more people than officially reported are likely to have had SARS-CoV-2 infections which are unaccounted for. Such a phenomenon would lend support to our suggestion that some populations in Africa may exhibit a blunted, pro-inflammatory adaptive response to SARS-CoV-2 infection. Currently, ongoing works across the 16 administrative regions of Ghana report a SARS-CoV-2 antibody seroprevalence range of approximately 26–57 % as of October 2021 (unpublished work from Rockefeller Foundation Grant Number: 2021 HTH 006).

Post-acute sequelae of COVID-19 lends credence to the suggestion that SARS-CoV-2 infection alters the inflammatory state. Alongside efforts to procure vaccines, therefore, it is just as important that Africa appreciates the potential impact of the apparently common but asymptomatic infections which likely have resulted in widespread natural inoculation. It is necessary to understand what changes in inflammatory state occur post SARS-CoV-2 infection in our populations, to help to characterize and preempt the effects on public health.

Data availability

No data are associated with this article.

Authors’ contributions

Daniel Oduro-Mensah: Conceptualization, Writing – original draft, Writing – review and editing. Ebenezer Oduro-Mensah: Writing – original draft, Writing – review and editing. Peter Quashie: Writing – review and editing. Gordon Akanzuwine Awandare: Writing – review and editing. Laud Kenneth Okine: Writing – original draft, Writing – review and editing.

Acknowledgements

The authors acknowledge the contributions of Nana Tawiah Ghunney and Stephanie Nanelle Hammond to the preparation of this manuscript.

References

  • 1.  WHO Coronavirus (COVID-19) Dashboard|WHO Coronavirus (COVID-19) Dashboard With Vaccination Data. Accessed June 23, 2021. Reference Source
  • 2.  Africa ‘has highest COVID-19 death rate of critically ill’ - Sub-Saharan Africa. Accessed June 23, 2021. Reference Source
  • 3.  Biccard BM, Gopalan PD, Miller M, et al.: Patient care and clinical outcomes for patients with COVID-19 infection admitted to African high-care or intensive care units (ACCCOS): a multicentre, prospective, observational cohort study. Lancet. 2021; 397(10288): 1885–1894. Publisher Full Text
  • 4.  World Population Clock: 7.9 Billion People (2021) - Worldometer. Accessed March 15, 2021. Reference Source
  • 5.  Coronavirus deaths by country in Africa 2021|Statista. Accessed June 23, 2021. Reference Source
  • 6.  Germany declares a Covid “third wave” has begun; Italy set for Easter lockdown. Accessed March 16, 2021. Reference Source
  • 7.  Europe is struggling to contain the third wave of the epidemic. - CNN. Accessed March 16, 2021. Reference Source
  • 8.  Third Covid wave sweeps across EU and forces new restrictions|Coronavirus|The Guardian. Accessed March 16, 2021. Reference Source
  • 9.  France Battles a Third Wave of COVID Infections|Voice of America - English. Accessed March 16, 2021. Reference Source
  • 10.  Risk of COVID-19 surge threatens Africa’s health facilities|WHO|Regional Office for Africa. Accessed July 4, 2021. Reference Source
  • 11.  Africa faces steepest COVID-19 surge yet|WHO|Regional Office for Africa. Accessed July 4, 2021. Reference Source
  • 12.  Coronavirus cases by country in Africa 2021|Statista. Accessed March 12, 2021. Reference Source
  • 13.  COVID19_Cases. Accessed March 12, 2021. Reference Source
  • 14.  WHO Coronavirus (COVID-19) Dashboard|WHO Coronavirus (COVID-19) Dashboard With Vaccination Data. Accessed July 4, 2021. Reference Source
  • 15.  Coronavirus Disease 2019 (COVID-19) – Africa CDC. Accessed August 16, 2021. Reference Source
  • 16.  Population of Africa (2021) - Worldometer. Accessed July 11, 2021. Reference Source
  • 17.  Napoli PE, Nioi M: Global Spread of Coronavirus Disease 2019 and Malaria: An Epidemiological Paradox in the Early Stage of A Pandemic. J. Clin. Med. 2020; 9(4): 1138. PubMed Abstract | Publisher Full Text | Free Full Text
  • 18.  Mbow M, Lell B, Jochems SP, et al.: COVID-19 in Africa: Dampening the storm?. Science (New York, N.Y.). 2020; 369(6504): 624–626. PubMed Abstract | Publisher Full Text
  • 19.  Diop BZ, Ngom M, Biyong CP, et al.: The relatively young and rural population may limit the spread and severity of COVID-19 in Africa: a modelling study. BMJ Glob. Health. 2020; 5(5): e002699. PubMed Abstract | Publisher Full Text | Free Full Text
  • 20.  Adams J, MacKenzie MJ, Amegah AK, et al.: The Conundrum of Low COVID-19 Mortality Burden in sub-Saharan Africa: Myth or Reality?. Global Health: Science and Practice. Published online July 30, 2021; 9: 433–443. Publisher Full Text
  • 21.  Gendrot M, Duflot I, Boxberger M, et al.: Antimalarial artemisinin-based combination therapies (ACT) and COVID-19 in Africa: in vitro inhibition of SARS-CoV-2 replication by mefloquine-artesunate.Published online 2020; 99: 437–440. Publisher Full Text
  • 22.  Why Africa’s COVID-19 Outbreak Isn’t So Bad|Time. Accessed March 12, 2021. Reference Source
  • 23.  Coronavirus in Africa: Five reasons why Covid-19 has been less deadly than elsewhere - BBC News. Accessed March 12, 2021. Reference Source
  • 24.  Njenga MK, Dawa J, Nanyingi M, et al.: Why is there low morbidity and mortality of COVID-19 in Africa?. Am. J. Trop. Med. Hyg. 2020; 103(2): 564–569. PubMed Abstract | Publisher Full Text | Free Full Text
  • 25.  Tso FY, Lindege SJ, Pena PB, et al.: High prevalence of pre-existing serological cross-reactivity against severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) in sub-Saharan Africa. International journal of infectious diseases: IJID: official publication of the International Society for Infectious Diseases. 2021; 102: 577–583. PubMed Abstract | Publisher Full Text | Free Full Text
  • 26.  Why Africa’s experience with COVID-19 has been atypical so far. Accessed March 12, 2021. Reference Source
  • 27.  Kusi KA, Frimpong A, Partey FD, et al.: High infectious disease burden as a basis for the observed high frequency of asymptomatic SARS-CoV-2 infections in sub-Saharan Africa. AAS Open Research. 2021; 4: 2. Publisher Full Text
  • 28.  Fonte L, Acosta A, Sarmiento ME, et al.: COVID-19 Lethality in Sub-Saharan Africa and Helminth Immune Modulation. Front. Immunol. 2020; 11: 2459. Publisher Full Text
  • 29.  Naidoo P, Ghazi T, Chuturgoon AA, et al.: SARS-CoV-2 and helminth co-infections, and environmental pollution exposure: An epidemiological and immunological perspective. Environ. Int. 2021; 156: 106695. PubMed Abstract | Publisher Full Text | Free Full Text
  • 30.  Malaria cases: estimated country share 2018|Statista. Accessed July 5, 2021. Reference Source
  • 31.  Ademolue TW, Aniweh Y, Kusi KA, et al.: Patterns of inflammatory responses and parasite tolerance vary with malaria transmission intensity. Malar. J. 2017; 16(1): 145. PubMed Abstract | Publisher Full Text | Free Full Text
  • 32.  Moncunill G, Mayor A, Jiménez A, et al.: Cytokine and Antibody Responses to Plasmodium falciparum in Naïve Individuals during a First Malaria Episode: Effect of Age and Malaria Exposure. Beeson JG, ed. PLoS One. 2013; 8(2): e55756. PubMed Abstract | Publisher Full Text | Free Full Text
  • 33.  Jagannathan P, Kim CC, Greenhouse B, et al.: Loss and dysfunction of Vδ2+γδ T cells are associated with clinical tolerance to malaria. Sci. Transl. Med. 2014; 6(251): 251ra117. PubMed Abstract | Publisher Full Text | Free Full Text
  • 34.  Doolan DL, Dobaño C, Baird JK: Acquired immunity to Malaria. Clin. Microbiol. Rev. 2009; 22(1): 13–36. PubMed Abstract | Publisher Full Text | Free Full Text
  • 35.  Schofield L, Mueller I: Clinical Immunity to Malaria. Curr. Mol. Med. 2006; 6(2): 205–221. PubMed Abstract | Publisher Full Text
  • 36.  Portugal S, Moebius J, Skinner J, et al.: Exposure-Dependent Control of Malaria-Induced Inflammation in Children. Kazura JW, ed. PLoS Pathog. 2014; 10(4): e1004079. PubMed Abstract | Publisher Full Text | Free Full Text
  • 37.  Farrington L, Vance H, Rek J, et al.: Both inflammatory and regulatory cytokine responses to malaria are blunted with increasing age in highly exposed children. Malar. J. 2017; 16(1): 499. PubMed Abstract | Publisher Full Text | Free Full Text
  • 38.  Boström S, Giusti P, Arama C, et al.: Changes in the levels of cytokines, chemokines and malaria-specific antibodies in response to Plasmodium falciparum infection in children living in sympatry in Mali. Malar. J. 2012; 11: PubMed Abstract | Publisher Full Text | Free Full Text
  • 39.  D’Ombrain MC, Robinson LJ, Stanisic DI, et al.: Association of early interferon-γ production with immunity to clinical malaria: A longitudinal study among Papua New Guinean children. Clin. Infect. Dis. 2008; 47(11): 1380–1387. PubMed Abstract | Publisher Full Text
  • 40.  Lei X, Dong X, Ma R, et al.: Activation and evasion of type I interferon responses by SARS-CoV-2. Nat. Commun. 2020; 11(1): 1–12. Publisher Full Text
  • 41.  SARS-CoV-2 delays interferon signaling in host cells. Accessed March 12, 2021. Reference Source
  • 42.  Wei JH, Nan ZH, Feng MQ, et al.: SARS-CoV-2 Orf9b suppresses type I interferon responses by targeting TOM70. Cell. Mol. Immunol. 2020; 17(9): 998–1000. PubMed Abstract | Publisher Full Text | Free Full Text
  • 43.  Stertz S, Hale BG: Interferon system deficiencies exacerbating severe pandemic virus infections. Trends Microbiol. Published online 2021; 29: 973–982. Publisher Full Text
  • 44.  Zhang Q, Liu Z, Moncada-Velez M, et al.: Inborn errors of type I IFN immunity in patients with life-threatening COVID-19. Science. 2020; 370(6515) PubMed Abstract | Publisher Full Text | Free Full Text
  • 45.  Yu C, Zhou M, Liu Y, et al.: Characteristics of asymptomatic COVID-19 infection and progression: A multicenter, retrospective study. Virulence. 2020; 11(1): 1006–1014. PubMed Abstract | Publisher Full Text | Free Full Text
  • 46.  Choi YH, Jin N, Kelly F, et al.: Elevation of alanine aminotransferase activity occurs after activation of the cell-death signaling initiated by pattern-recognition receptors but before activation of cytolytic effectors in NK or CD8+ T cells in the liver during acute HCV infection. PLoS One. 2016; 11(10): e0165533. PubMed Abstract | Publisher Full Text | Free Full Text
  • 47.  Trindade Bezerra JM, Soeiro Barbosa D, Rogerlândio Martins-Melo F: Changes in malaria patterns in Brazil over 28 years (1990–2017): results from the Global Burden of Disease Study 2017.Published online 2020. Publisher Full Text
  • 48.  Brazil: number of COVID-19 deaths, by state 2021|Statista. Accessed July 12, 2021. Reference Source
  • 49.  Coronavirus cases worldwide by country|Statista. Accessed July 12, 2021. Reference Source
  • 50.  Hong M, Bertoletti A: Tolerance and immunity to pathogens in early life: insights from HBV infection. Semin. Immunopathol. 2017; 39(6): 643–652. PubMed Abstract | Publisher Full Text | Free Full Text
  • 51.  Yap GS, Gause WC: Helminth infections induce tissue tolerance mitigating immunopathology but enhancing microbial pathogen susceptibility. Front. Immunol. 2018; 9(Oct): 2135. Publisher Full Text
  • 52.  King IL, Li Y: Host-parasite interactions promote disease tolerance to intestinal helminth infection. Front. Immunol. 2018; 9(Sep): 2128. Publisher Full Text
  • 53.  Ma Z, Li P, Ji Y, et al.: Cross-reactivity towards SARS-CoV-2: the potential role of low-pathogenic human coronaviruses. The Lancet Microbe. 2020; 1(4): e151. PubMed Abstract | Publisher Full Text | Free Full Text
  • 54.  Guo L, Wang Y, Kang L, et al.: Cross-reactive antibody against human coronavirus OC43 spike protein correlates with disease severity in COVID-19 patients: a retrospective study. Emerging Microbes and Infections. 2021; 10(1): 664–676. PubMed Abstract | Publisher Full Text | Free Full Text
  • 55.  Rönnbäck C, Hansson E: The Importance and Control of Low-Grade Inflammation Due to Damage of Cellular Barrier Systems That May Lead to Systemic Inflammation. Front. Neurol. 2019; 10(MAY): 533. Publisher Full Text
  • 56.  León-Pedroza JI, González-Tapia LA, del Olmo-Gil E , et al.: Low-grade systemic inflammation and the development of metabolic diseases: From the molecular evidence to the clinical practice. Cirugía y Cirujanos (English Edition). 2015; 83(6): 543–551. Publisher Full Text
  • 57.  Krabbe KS, Pedersen M, Bruunsgaard H: Inflammatory mediators in the elderly. Exp. Gerontol. 2004; 39(5): 687–699. PubMed Abstract | Publisher Full Text
  • 58.  Calder PC, Bosco N, Bourdet-Sicard R, et al.: Health relevance of the modification of low grade inflammation in ageing (inflammageing) and the role of nutrition. Ageing Res. Rev. 2017; 40: 95–119. PubMed Abstract | Publisher Full Text
  • 59.  Castro AM, Macedo-de la Concha LE, Pantoja-Meléndez CA: Low-grade inflammation and its relation to obesity and chronic degenerative diseases. Revista Médica del Hospital General de México. 2017; 80(2): 101–105. Publisher Full Text
  • 60.  Minihane AM, Vinoy S, Russell WR, et al.: Low-grade inflammation, diet composition and health: Current research evidence and its translation. Br. J. Nutr. 2015; 114(7): 999–1012. PubMed Abstract | Publisher Full Text | Free Full Text
  • 61.  Rönnbäck C, Hansson E: The Importance and Control of Low-Grade Inflammation Due to Damage of Cellular Barrier Systems That May Lead to Systemic Inflammation. Front. Neurol. 2019; 10(May): 533. Publisher Full Text
  • 62.  The Rise and Rise of Chronic Diseases in Africa - Sanofi. Accessed March 14, 2021. Reference Source
  • 63.  de-Graft Aikins A, Addo J, Ofei F, et al.: Ghana’s burden of chronic non-communicable diseases: future directions in research, practice and policy. Ghana Med. J. 2012; 46(2 Suppl): 1–3. Accessed March 19, 2021. Reference Source
  • 64.  Moro-García MA, Mayo JC, Sainz RM, et al.: Influence of inflammation in the process of T lymphocyte differentiation: Proliferative, metabolic, and oxidative changes. Front. Immunol. 2018; 9(Mar): 1. Publisher Full Text
  • 65.  Ciornei RT: Prevention of Severe Coronavirus Disease 2019 Outcomes by Reducing Low-Grade Inflammation in High-Risk Categories. Front. Immunol. 2020; 11: 1762. Publisher Full Text
  • 66.  Chiappetta S, Sharma AM, Bottino V, et al.: COVID-19 and the role of chronic inflammation in patients with obesity. Int. J. Obes. 2020; 44(8): 1790–1792. Publisher Full Text
  • 67.  Huizinga GP, Singer BH, Singer K: The collision of meta-inflammation and SARS-CoV-2 pandemic infection. Endocrinology (United States). 2020; 161(11): 1–10. PubMed Abstract | Publisher Full Text | Free Full Text
  • 68.  Kim J, Nam JH: Insight into the relationship between obesity-induced low-level chronic inflammation and COVID-19 infection. Int. J. Obes. 2020; 44(7): 1541–1542. PubMed Abstract | Publisher Full Text | Free Full Text
  • 69.  Tskhay A, Yezhova A, Alibek K: COVID-19 Pandemic: Is Chronic Inflammation a Major Cause of Death?.Publisher Full Text
  • 70.  Akbar AN, Gilroy DW: Aging immunity may exacerbate COVID-19. Science. 2020; 369(6501): 256–257. PubMed Abstract | Publisher Full Text
  • 71.  Mostaghim A, Sinha P, Bielick C, et al.: Clinical outcomes and inflammatory marker levels in patients with Covid-19 and obesity at an inner-city safety net hospital. Zivkovic AR, ed. PLoS One. 2020; 15(12): e0243888. PubMed Abstract | Publisher Full Text | Free Full Text
  • 72.  Honce R, Schultz-Cherry S: Impact of obesity on influenza A virus pathogenesis, immune response, and evolution. Front. Immunol. 2019; 10(May): 1071. Publisher Full Text
  • 73.  Green WD, Beck MA: Obesity impairs the adaptive immune response to influenza virus. Ann. Am. Thorac. Soc. 2017; 14(Suppl 5): S406–S409. PubMed Abstract | Publisher Full Text | Free Full Text
  • 74.  Dicker D, Bettini S, Farpour-Lambert N, et al.: Obesity and COVID-19: The Two Sides of the Coin. Obes. Facts. 2020; 13(4): 430–438. PubMed Abstract | Publisher Full Text | Free Full Text
  • 75.  Obesity and COVID-19 Severity in a Designated Hospital in Shenzhen, China A total of 383 consecutively hospitalized patients with COVID.Published online 2020. Publisher Full Text
  • 76.  Green WD, Beck MA: Obesity impairs the adaptive immune response to influenza virus. Ann. Am. Thorac. Soc. 2017; 14: S406–S409. PubMed Abstract | Publisher Full Text | Free Full Text
  • 77.  Contributor: Links Between COVID-19 Comorbidities, Mortality Detailed in FAIR Health Study. Accessed March 16, 2021. Reference Source
  • 78.  Gupta R, Agrawal R, Bukhari Z, et al.: Higher comorbidities and early death in hospitalized African-American patients with Covid-19. BMC Infect. Dis. 2021; 21(1): 78. PubMed Abstract | Publisher Full Text | Free Full Text
  • 79.  Age, sex, comorbidities impact outcomes after COVID-19 hospitalization. Accessed March 16, 2021. Reference Source
  • 80.  D’ascanio M, Innammorato M, Pasquariello L, et al.: Age is not the only risk factor in COVID-19: the role of comorbidities and of long staying in residential care homes. BMC Geriatr. 2021; 21(1): 63. PubMed Abstract | Publisher Full Text | Free Full Text
  • 81.  Mostaghim A, Sinha P, Bielick C, et al.: Clinical outcomes and inflammatory marker levels in patients with Covid-19 and obesity at an inner-city safety net hospital. PLoS One. 2020; 15(12 December): e0243888. PubMed Abstract | Publisher Full Text | Free Full Text
  • 82.  Patients with COVID-19 and obesity have poor outcomes not driven by inflammation|EurekAlert! Science News. Accessed March 12, 2021. Reference Source
  • 83.  Kooistra EJ, de Nooijer AH , Claassen WJ, et al.: A higher BMI is not associated with a different immune response and disease course in critically ill COVID-19 patients. Int. J. Obes. 2021; 45(3): 687–694. PubMed Abstract | Publisher Full Text | Free Full Text
  • 84.  Pizarro-Sánchez MS, Avello A, Mas-Fontao S, et al.: Clinical Features of Asymptomatic SARS-CoV-2 Infection in Hemodialysis Patients. Kidney Blood Press. Res. 2021; 46(1): 1–9. Publisher Full Text
  • 85.  Polack FP, Thomas SJ, Kitchin N, et al.: Safety and Efficacy of the BNT162b2 mRNA Covid-19 Vaccine. N. Engl. J. Med. 2020; 383(27): 2603–2615. PubMed Abstract | Publisher Full Text | Free Full Text
  • 86.  Ramasamy MN, Minassian AM, Ewer KJ, et al.: Safety and immunogenicity of ChAdOx1 nCoV-19 vaccine administered in a prime-boost regimen in young and old adults (COV002): a single-blind, randomised, controlled, phase 2/3 trial. Lancet. 2020; 396(10267): 1979–1993. PubMed Abstract | Publisher Full Text | Free Full Text
  • 87.  Anderson EJ, Rouphael NG, Widge AT, et al.: Safety and Immunogenicity of SARS-CoV-2 mRNA-1273 Vaccine in Older Adults. N. Engl. J. Med. 2020; 383(25): 2427–2438. PubMed Abstract | Publisher Full Text | Free Full Text
  • 88.  Sanada F, Taniyama Y, Muratsu J, et al.: Source of Chronic Inflammation in Aging. Front. Cardiovasc. Med. 2018; 5: 12. Publisher Full Text
  • 89.  Franceschi C, Campisi J: Chronic inflammation (Inflammaging) and its potential contribution to age-associated diseases. J. Gerontol. A Biol. Sci. Med. Sci. 2014; 69: S4–S9. Publisher Full Text
  • 90.  Panda A, Qian F, Mohanty S, et al.: Age-Associated Decrease in TLR Function in Primary Human Dendritic Cells Predicts Influenza Vaccine Response. J. Immunol. 2010; 184(5): 2518–2527. PubMed Abstract | Publisher Full Text | Free Full Text
  • 91.  Guarner V, Rubio-Ruiz ME: Aging and Health-A Systems Biology Perspective. Interdiscipl Top Gerontol Basel, Karger. 2015; 40: 99–106. Publisher Full Text
  • 92.  Grignolio A, Mishto M, Caetano Faria AM, et al.: Towards a liquid self: How time, geography, and life experiences reshape the biological identity. Front. Immunol. 2014; 5(Apr): 153. Publisher Full Text
  • 93.  Salvioli S, Monti D, Lanzarini C, et al.: Immune System, Cell Senescence, Aging and Longevity - Inflamm-Aging Reappraised.
  • 94.  Franceschi C, Capri M, Monti D, et al.: Inflammaging and anti-inflammaging: A systemic perspective on aging and longevity emerged from studies in humans. Mech. Ageing Dev. 2007; 128(1): 92–105. PubMed Abstract | Publisher Full Text
  • 95.  Morrisette-Thomas V, Cohen AA, Fülöp T, et al.: Inflamm-aging does not simply reflect increases in pro-inflammatory markers. Mech. Ageing Dev. 2014; 139(1): 49–57. PubMed Abstract | Publisher Full Text | Free Full Text
  • 96.  Daher A, Balfanz P, Aetou M, et al.: Clinical course of COVID-19 patients needing supplemental oxygen outside the intensive care unit. Sci. Rep. 2021; 11(1): 2256. PubMed Abstract | Publisher Full Text | Free Full Text
  • 97.  Klein H, Asseo K, Karni N, et al.: Onset, duration and unresolved symptoms, including smell and taste changes, in mild COVID-19 infection: a cohort study in Israeli patients. Clin. Microbiol. Infect. 2021; 27: 769–774. Publisher Full Text
  • 98.  Carvalho-Schneider C, Laurent E, Lemaignen A, et al.: Follow-up of adults with noncritical COVID-19 two months after symptom onset. Clin. Microbiol. Infect. 2021; 27(2): 258–263. PubMed Abstract | Publisher Full Text | Free Full Text
  • 99.  Stavem K, Ghanima W, Olsen MK, Gilboe HM, et al.: Persistent symptoms 1.5-6 months after COVID-19 in non-hospitalised subjects: A population-based cohort study. Thorax. Published online December 3, 2020; 76: 405–407. Publisher Full Text
  • 100.  Ladds E, Rushforth A, Wieringa S, et al.: Persistent symptoms after Covid-19: qualitative study of 114 “long Covid” patients and draft quality principles for services. BMC Health Serv. Res. 2020; 20(1): 1144. PubMed Abstract | Publisher Full Text | Free Full Text
  • 101.  Huang C, Huang L, Wang Y, et al.: 6-month consequences of COVID-19 in patients discharged from hospital: a cohort study. Lancet. 2021; 397(10270): 220–232. PubMed Abstract | Publisher Full Text | Free Full Text
  • 102.  Garrigues E, Janvier P, Kherabi Y, et al.: Post-discharge persistent symptoms and health-related quality of life after hospitalization for COVID-19. J. Infect. 2020; 81(6): e4–e6. PubMed Abstract | Publisher Full Text | Free Full Text
  • 103.  Chopra V, Flanders SA, O’Malley M, et al.: Sixty-Day Outcomes Among Patients Hospitalized With COVID-19. Ann. Intern. Med. Published online November 11, 2020. Publisher Full Text
  • 104.  Carfì A, Bernabei R, Landi F: Persistent symptoms in patients after acute COVID-19. JAMA. 2020; 324(6): 603–605. PubMed Abstract | Publisher Full Text | Free Full Text
  • 105.  Lasselin J, Magne E, Beau C, et al.: Low-grade inflammation is a major contributor of impaired attentional set shifting in obese subjects. Brain Behav. Immun. 2016; 58: 63–68. Publisher Full Text
  • 106.  Quashie PK, Mutungi JK, Dzabeng F, et al.: Trends of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) antibody prevalence in selected regions across Ghana. Wellcome Open Res. 2021; 6: 173. Publisher Full Text
  • 107.  COVID-19 Situation Dashboard|Ghana. Accessed September 28, 2021. Reference Source
  • 108.  Adetifa IMO, Uyoga S, Gitonga JN, et al.: Temporal trends of SARS-CoV-2 seroprevalence during the first wave of the COVID-19 epidemic in Kenya. Nat. Commun. 2021; 12(1): 3966–3966. PubMed Abstract | Publisher Full Text | Free Full Text
  • 109.  Chisale MRO, Ramazanu S, Mwale SE, et al.: Seroprevalence of anti-SARS-CoV-2 antibodies in Africa: A systematic review and meta-analysis. Rev. Med. Virol. Published online July 6, 2021. Publisher Full Text

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Oduro-Mensah D, Oduro-Mensah E, Quashie P et al. Explaining the unexpected COVID-19 trends and potential impact across Africa. [version 1; peer review: 1 approved with reservations] F1000Research 2021, 10:1177 (https://doi.org/10.12688/f1000research.74363.1)
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Reviewer Report 30 Aug 2022
Sankha Shubhra Chakrabarti, Department of Geriatric Medicine, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, India 
Approved with Reservations
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https://doi.org/10.5256/f1000research.78107.r146899
This is an interesting hypothesis article. There are some minor grammatical errors. Please correct those.
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Chakrabarti SS. Reviewer Report For: Explaining the unexpected COVID-19 trends and potential impact across Africa. [version 1; peer review: 1 approved with reservations]. F1000Research 2021, 10:1177 (https://doi.org/10.5256/f1000research.78107.r146899)
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  • Author Response 21 Nov 2022
    Daniel Oduro-Mensah, West African Center for Cell Biology of Infectious Pathogens, College of Basic and Applied Sciences, University of Ghana, Accra, Ghana
    21 Nov 2022
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    The authors sincerely appreciate the time and effort the reviewer has spent to make the report better.
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  • Author Response 21 Nov 2022
    Daniel Oduro-Mensah, West African Center for Cell Biology of Infectious Pathogens, College of Basic and Applied Sciences, University of Ghana, Accra, Ghana
    21 Nov 2022
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    The authors sincerely appreciate the time and effort the reviewer has spent to make the report better.
    We take note of the reviewer’s comments and respond as follows:
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The paper is scientifically sound in its current form and only minor, if any, improvements are suggested
Approved with reservations
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Fundamental flaws in the paper seriously undermine the findings and conclusions

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  1. Sankha Shubhra Chakrabarti, Banaras Hindu University, Varanasi, India
  2. Kurnia Fitri Jamil, Universitas Syiah Kuala, Banda Aceh, Indonesia

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    Alongside their report, reviewers assign a status to the article:
    Approved - the paper is scientifically sound in its current form and only minor, if any, improvements are suggested
    Approved with reservations - A number of small changes, sometimes more significant revisions are required to address specific details and improve the papers academic merit.
    Not approved - fundamental flaws in the paper seriously undermine the findings and conclusions
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