The current outbreak of the novel coronavirus SARS‐CoV‐2 (coronavirus disease 2019;
previously 2019‐nCoV), epi‐centred in Hubei Province of the People’s Republic of China,
has spread to many other countries. On 30. January 2020, the WHO Emergency Committee
declared a global health emergency based on growing case notification rates at Chinese
and international locations. The case detection rate is changing daily and can be
tracked in almost real time on the website provided by Johns Hopkins University 1
and other forums. As of midst of February 2020, China bears the large burden of morbidity
and mortality, whereas the incidence in other Asian countries, in Europe and North
America remains low so far.
Coronaviruses are enveloped, positive single‐stranded large RNA viruses that infect
humans, but also a wide range of animals. Coronaviruses were first described in 1966
by Tyrell and Bynoe, who cultivated the viruses from patients with common colds 2.
Based on their morphology as spherical virions with a core shell and surface projections
resembling a solar corona, they were termed coronaviruses (Latin: corona = crown).
Four subfamilies, namely alpha‐, beta‐, gamma‐ and delta‐coronaviruses exist. While
alpha‐ and beta‐coronaviruses apparently originate from mammals, in particular from
bats, gamma‐ and delta‐viruses originate from pigs and birds. The genome size varies
between 26 kb and 32 kb. Among the seven subtypes of coronaviruses that can infect
humans, the beta‐coronaviruses may cause severe disease and fatalities, whereas alpha‐coronaviruses
cause asymptomatic or mildly symptomatic infections. SARS‐CoV‐2 belongs to the B lineage
of the beta‐coronaviruses and is closely related to the SARS‐CoV virus 3, 4. The major
four structural genes encode the nucleocapsid protein (N), the spike protein (S),
a small membrane protein (SM) and the membrane glycoprotein (M) with an additional
membrane glycoprotein (HE) occurring in the HCoV‐OC43 and HKU1 beta‐coronaviruses
5. SARS‐CoV‐2 is 96% identical at the whole‐genome level to a bat coronavirus 4.
SARS‐CoV‐2 apparently succeeded in making its transition from animals to humans on
the Huanan seafood market in Wuhan, China. However, endeavours to identify potential
intermediate hosts seem to have been neglected in Wuhan and the exact route of transmission
urgently needs to be clarified.
The initial clinical sign of the SARS‐CoV‐2‐related disease COVID‐19 which allowed
case detection was pneumonia. More recent reports also describe gastrointestinal symptoms
and asymptomatic infections, especially among young children 6. Observations so far
suggest a mean incubation period of five days 7 and a median incubation period of
3 days (range: 0–24 days) 8. The proportion of individuals infected by SARS‐CoV‐2
who remain asymptomatic throughout the course of infection has not yet been definitely
assessed. In symptomatic patients, the clinical manifestations of the disease usually
start after less than a week, consisting of fever, cough, nasal congestion, fatigue
and other signs of upper respiratory tract infections. The infection can progress
to severe disease with dyspnoea and severe chest symptoms corresponding to pneumonia
in approximately 75% of patients, as seen by computed tomography on admission 8. Pneumonia
mostly occurs in the second or third week of a symptomatic infection. Prominent signs
of viral pneumonia include decreased oxygen saturation, blood gas deviations, changes
visible through chest X‐rays and other imaging techniques, with ground glass abnormalities,
patchy consolidation, alveolar exudates and interlobular involvement, eventually indicating
deterioration. Lymphopenia appears to be common, and inflammatory markers (C‐reactive
protein and proinflammatory cytokines) are elevated.
Recent investigations of 425 confirmed cases demonstrate that the current epidemic
may double in the number of affected individuals every seven days and that each patient
spreads infection to 2.2 other individuals on average (R0) 6. Estimates from the SARS‐CoV
outbreak in 2003 reported an R0 of 3 9. A recent data‐driven analysis from the early
phase of the outbreak estimates a mean R0 range from 2.2 to 3.58 10.
Dense communities are at particular risk and the most vulnerable region certainly
is Africa, due to dense traffic between China and Africa. Very few African countries
have sufficient and appropriate diagnostic capacities and obvious challenges exist
to handle such outbreaks. Indeed, the virus might soon affect Africa. WHO has identified
13 top‐priority countries (Algeria, Angola, Cote d’Ivoire, the Democratic Republic
of the Congo, Ethiopia, Ghana, Kenya, Mauritius, Nigeria, South Africa, Tanzania,
Uganda, Zambia) which either maintain direct links to China or a high volume of travel
to China.
Recent studies indicate that patients ≥60 years of age are at higher risk than children
who might be less likely to become infected or, if so, may show milder symptoms or
even asymptomatic infection 7. As of 13. February 2020, the case fatality rate of
COVID‐19 infections has been approximately 2.2% (1370/60363; 13. February 2020, 06:53
PM CET); it was 9.6% (774/8096) in the SARS‐CoV epidemic 11 and 34.4% (858/2494) in
the MERS‐CoV outbreak since 2012 12.
Like other viruses, SARS‐CoV‐2 infects lung alveolar epithelial cells using receptor‐mediated
endocytosis via the angiotensin‐converting enzyme II (ACE2) as an entry receptor 4.
Artificial intelligence predicts that drugs associated with AP2‐associated protein
kinase 1 (AAK1) disrupting these proteins may inhibit viral entry into the target
cells 13. Baricitinib, used in the treatment of rheumatoid arthritis, is an AAK1 and
Janus kinase inhibitor and suggested for controlling viral replication 13. Moreover,
one in vitro and a clinical study indicate that remdesivir, an adenosine analogue
that acts as a viral protein inhibitor, has improved the condition in one patient
14, 15. Chloroquine, by increasing the endosomal pH required for virus‐cell fusion,
has the potential of blocking viral infection 15 and was shown to affect activation
of p38 mitogen‐activated protein kinase (MAPK), which is involved in replication of
HCoV‐229E 16. A combination of the antiretroviral drugs lopinavir and ritonavir significantly
improved the clinical condition of SARS‐CoV patients 17 and might be an option in
COVID‐19 infections. Further possibilities include leronlimab, a humanised monoclonal
antibody (CCR5 antagonist), and galidesivir, a nucleoside RNA polymerase inhibitor,
both of which have shown survival benefits in several deadly virus infections and
are being considered as potential treatment candidates 18. Repurposing these available
drugs for immediate use in treatment in SARS‐CoV‐2 infections could improve the currently
available clinical management. Clinical trials presently registered at ClinicalTrials.gov
focus on the efficacy of remdesivir, immunoglobulins, arbidol hydrochloride combined
with interferon atomisation, ASC09F+Oseltamivir, ritonavir plus oseltamivir, lopinavir
plus ritonavir, mesenchymal stem cell treatment, darunavir plus cobicistat, hydroxychloroquine,
methylprednisolone and washed microbiota transplantation 19.
Given the fragile health systems in most sub‐Saharan African countries, new and re‐emerging
disease outbreaks such as the current COVID‐19 epidemic can potentially paralyse health
systems at the expense of primary healthcare requirements. The impact of the Ebola
epidemic on the economy and healthcare structures is still felt five years later in
those countries which were affected. Effective outbreak responses and preparedness
during emergencies of such magnitude are challenging across African and other lower‐middle‐income
countries. Such situations can partly only be mitigated by supporting existing regional
and sub‐Saharan African health structures.