Abstract
COVID-19 has undergone rapid spread worldwide, with the number of
infected patients and death events being increased at exponential rates,
and thus considered an epidemic disaster. However, SARS-CoV-2 has
reduced case-fatality rate and enhanced transmission capacity that favor
its propagation and make it evolutionarily more advanced than the other
coronaviruses. Further, SARS-CoV-2 preserves virulence to certain
patients while keeping some patients symptom-free. It is hypothesized
here that SARS-CoV-2 functions as a natural selection pressure for human
evolution. That is, COVID-19 is an epidemic disaster at the individual
level but may be evolutionarily beneficial for the human at the
population level, and survived individuals from SARS-CoV-2 infection may
be more tolerable to redox pressure and not suffer anymore from diseases
such as hypertension if without external intervention.
Keywords: COVID-19, SARS-CoV-2, evolution, symbiosis, herd
immunity
Word count: 964
Coronavirus disease 2019 (COVID-19), a novel pneumonia that is caused by
Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), has
undergone rapid spread worldwide, taken away the life of many civilians,
and thus considered an epidemic disaster.[1]
Recent findings indicate that the outbreak of COVID-19 in different
countries may not share the same pathogen origin,[2] some of which
were suspected to have already appeared in other places in the world
prior to the outbreak of COVID-19 in China. Therefore, COVID-19 may be a
global health problem ‘simultaneously’ appeared at different locations
on the earth in this era. While some patients are symptom-free, elder
individuals with comorbidities especially hypertension have, in general,
a higher case-fatality rate that may be a result of either weaker immune
protection or higher redox level in these patients.[3, 4] In
addition, evidence was reported on the involvement of human deaminases
APOBECs/ADARs in SARS-CoV-2 transcriptome editing,[5] suggesting the
attempt of SARS-CoV-2 in human genome integration and host natural
response; and SARS-CoV-2 was demonstrated as an outcome of natural
selection and evolution.[6] These make us wonder, is COVID-19 a pure
epidemic disaster? Does it impose any global selection pressure
beneficial for humankind evolution?
Co-evolving with viruses has long been part of the human evolution
history, with up to 8% human genome sequences being originated from
viruses.[7] The fate of viruses is either extinction or symbiosis
which is determined by its virulence and transmission rate. High
virulence would cause extinction of either its own or the host, and
unless viruses could find another species for co-existence, the death of
the host is equivalent to the end of its own fate. Low virulence and low
transmission may easily lead virus to extinction. Low virulence and high
transmission are beneficial for virus propagation, and viruses having
these features are evolutionarily more advanced and are more likely to
evolve into amensalism or commensalism with the hosts. External
interventions may not eradicate these viruses but rather accelerate
their evolutionary process. Hepatitis B virus (HBV) is an example of
amensalism that may cause cirrhosis and liver cancer despite its long
co-existence with the host; and human endogenous retrovirus W (HERV-W)
is a good example of commensalism, as after integrating into human
genome, the new gene it created, ERVWE1 , encodes syncytin that
plays critical roles in human embryo placentation.
SARS-CoV-2 is less virulent and more transmissive than SARS-CoV and
MERS-CoV that outbroke in Asia and Middle East, respectively, in 2003
and 2012,[3] fulfilling the criteria of evolving into symbiosis with
human. On one hand, reduced case-fatality rate and enhanced transmission
capacity of SARS-CoV-2 favor its propagation and make it evolutionarily
more advanced than the other coronaviruses. On the other hand,
SARS-CoV-2 is lethal to certain patients but keeps some symptom-free
that makes it function as a natural selection pressure for human
evolution, the same as what has enabled human evolution from, e.g.,Homo habilis to Homo sapiens denisova . Importantly,
COVID-19 is under vigorous medication control that may considerably
accelerate this process.
Whether SARS-CoV-2 will evolve into amensalism or commensalism depends
on whether human could co-evolve traits capable of tolerating its
virulence and whether the genome of SARS-CoV-2 would convey beneficial
effects to human once integrated into human genome. The existence of
symptom-free COVID-19 patients suggests the natural tolerance of
SARS-CoV-2 in some people. In addition, SARS-CoV-2 binds ACE2 that is
protective of the cardiovascular system and capable of maintaining redox
homeostasis. On redox stress that is typically imposed by viral
infection, ACE2 may be translocated into the nucleus to regulate the
expression of genes responsible for quenching elevated reactive species,
and thus convey protective effects to human vascular system. Thereby, by
integrating into human genome, SARS-CoV-2 may advance humankind towards
enhanced tolerance to redox stress and less likelihood of developing
hypertension that could be conceived as a disease of imbalanced redox
metabolism.[8] As a trend, it is reasonable to perceive the
establishment of commensalism between SARS-CoV-2 and human. Consistent
with this, a recent publication showed evidence on the evolvement of
SARS-CoV-2 towards reduced virulence.[9] Thereby, COVID-19 may not
be a disaster but rather represent a selection pressure towards human
evolution against diseases caused by redox imbalance such as
cardiovascular disorders.
Hypertension is the global leading cause of modality and represents the
most important factor predisposing the risk of developing cardiovascular
diseases.[10] Naturally low level of reactive species, high
tolerance to redox imbalance, or evolvement of mechanism that could
quench excess redox pressure are advantageous in surviving from
COVID-19. Individuals having such abilities primed in their genome or
gained such abilities via co-evolving with viruses will survive from
SARS-CoV-2 infection, and pass on their genetic information to the next
generations. These selected or evolved traits would make survivors less
likely to develop hypertension and cardiovascular diseases and thus
enjoy prolonged longevity. Though the outcome of this epidemic may be
favorable at the population level, the process suffers as the battle
between viruses and hosts during co-evolution is indispensable and
always at the sacrifice of the lives of many human beings at the
individual level.
The British government announced the concept of ‘herd immunity’[11]
which though raised debates, to some extent, is in agreement with the
concept of ‘population evolution’ here. Considering humanity and ethics,
we are well suggested to rescue the lives of all COVID-10 patients
including those severely infected. However, while we pray for those who
died from COVID-19, we should be optimistic on the future as SARS-CoV-2
helped enriching mankind with survivors primed with high tolerance to
redox pressure to some extent that may evolve additional traits
favorable for human health, and thus should encourage lightly infected
patients co-evolve with virus towards this potential genetic advance.
Investigations on the genetic traits and health condition of COVID-19
survivors and symptom-free carriers are encouraged to advance our
understandings on this epidemic.