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*Corresponding author: E-mail: sadeeqsheshe@yahoo.com; 
 
 
 

Asian Journal of Immunology 
 
3(1): 91-98, 2020; Article no.AJI.55971 
 

 
 

 

 

Mechanism of Antiviral Immune Response and 
COVID-19 Infection 

 
Sadeeq Sheshe1*, Abdullahi Nazifi1, A. M. Labbo2, G. M. Khalid3,  

Abubakar Yahya4, Umar Muhammad5 and Aliyu Musa Haruna6 
 

1
Department of Biochemistry, Kano University of Science and Technology, Wudil, Nigeria. 

2
Department of Biochemistry, Sokoto State University, Nigeria. 

3
Department of Pharmaceutics and Pharmaceutical Technology, Bayero University Kano, Nigeria. 

4
Department of Pediatrics, Muhammad Abdullahi Wase Specialist Hospital, Kano, Nigeria. 

5
Department of Pediatrics, Federal Medical Centre, Gusau, Nigeria. 

6
Department of Medicine, Aminu Kano Teaching Hospital, Bayero University Kano, Nigeria. 

 
Authors’ contributions  

 
This work was carried out in collaboration among all authors. Author SS designed the study. Authors 

AN and AML performed critical analysis of the literature. Author GMK analyzed the recent data 
updates. Authors AY and UM searched for the literature. Author AMH wrote the first draft of the 

manuscript. All authors read and approved the final manuscript. 
 

Article Information 
 

Editor(s): 
(1) Dr. Cynthia Aracely Alvizo Báez, Autonomous University of Nuevo Leon, Mexico. 

Reviewers: 
(1) Victor B. Oti, Nasarawa State University, Nigeria. 

(2) Pichon Maxime, University Hospital of Poitiers, France. 
Complete Peer review History: http://www.sdiarticle4.com/review-history/55971 

 
 
 
 

Received 23 March 2020  
Accepted 04 April 2020 
Published 09 April 2020 

 
 

ABSTRACT 
 

Immune systems are responsible for the body’s protection against invading foreign agents that 
could bring harm to normal cellular activities. Viral infection is one of the significant foreign attacks 
on the body and the immune system has developed key mechanisms to contain such attack. The 
recent pandemic of the Coronavirus disease 2019 (COVID-19) has stimulated studies on antiviral 
response with much emphasis on the Corona viruses. This disease caused by the novel Severe 
Acute Respiratory Syndrome-Coronavirus-2 (SARS-COV-2) has been shown to have evolved with 
mechanisms to evade the normal immune responses. As such, this review therefore critically 
apprised recent literature on mechanisms of antiviral responses emphasizing on the Coronaviruses 
particularly the SARS-COV-2.The paper also highlighted the current situation regarding studies to 
find cure and vaccine development against the COVID-19. 

Mini-review Article 



 
 
 
 

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92 

 

Keywords: Immunity; Corona virus; Covid-19; immune; antiviral; innate; adaptive; lymphocytes. 
 

1. INTRODUCTION 
 
The immune system is the major protective 
system of the body against invading foreign 
bodies and infectious agents [1]. Human immune 
system is one of the most critical and complex 
systems responsible for mediating response 
against foreign agents [2]. Such system could be 
the inborn innate immunity involving group of 
cells much organized up to organ levels that 
serve to protect the body against any infection. 
Such innate immune system involves one of the 
first line of immune response [3]. 
 
The innate immune system comprises of organs 
including the skin responsible for the major 
protection of the body [4]. Continuously, it 
includes group of cells protecting the body 
against any foreign invading material without any 
further categorization [4]. These cells mostly 
ferocious in their actions kill or damage the 
invading foreign body, release chemicals that 
ultimately kills the foreign agent [5]. 
 

Adaptive immunity on the other hand which is 
also referred to as the acquired immunity is the 
other type of immune response [6]. It is mostly 
concerned with detailed and more specific action 
against invading microbes, toxins and even 
mediating immune response between donor and 
recipient during organ or tissue transplants [7]. It 
is much controlled and specified form of 
immunity and involves key mechanisms for 
activation of different cells. This acquired 
immunity could mediate a cellular based 
response or humoral immunity [8]. 
 
Cell mediated immune response involves the 
activation of cells that could lead to destruction 
and elimination of the foreign bodies [9]. The cell 
mediated immune response comprises the key 
players; lymphocytes [10]. These cells 
particularly the T lymphocytes are responsible for 
the cell based immune responses.  The T 
lymphocytes (T-cells) mediate response through 
presentation of the antigens of the invading cells 
particularly in viral infections [11]. The 
presentation involves action of proteins that 
culminates in formation of histocompatibility 
complex with the antigenic material. Accordingly, 
the presentation of histocompatibility complex 
class I (MHC I) leads to activation of Cytotoxic T 
cells [12]. These cells are significant in cell based 
immune responses.  In essence, upon viral 
infection, the viral proteins are presented on the 

MHC I which in turn activates the cytotoxic T 
cells there by mounting a response against the 
virus [13]. 
 

Humoral immune response is associated with B 
lymphocytes activation and subsequent release 
of specially produced antibodies [14]. In terms of 
antigen presentation, the proteins of the invading 
agent are presented on MHC II thus leading to 
activation and subsequent proliferation of B-cells 
[12]. The B cells continue to produce antibodies 
otherwise known as Immunoglobulins and 
facilitation of Antigen-antibody complex formation 
[15]. This complex formation is paramount to 
elimination of the invading agent as the 
antibodies are specific towards the consequent 
antigen [16]. 
 

At the center of all these activations in the 
adaptive immunity are the Helper T-cells. They 
are referred to as architects of all immune 
responses [17]. The B-cells also develop into 
specialized Memory B-cells having the tendency 
to store the memory of the antigen which initially 
caused the immune response and subsequent 
production of the specified Antibodies [12]. With 
the current surge in the pandemic Corona virus 
disease-2019 (Covid19) which is ravaging the 
globe, this review critically discussed the current 
literature regarding antiviral immune response in 
humans with particular attention on the Covid19. 
Literature was extracted from Scopus, Web of 
Science, PubMed, and Embase using the 
following keywords; Coronavirus, Covid-19, 
Immune, Antiviral, Innate, Adaptive, 
Lymphocytes. 
 

2. MECHANISM of DIFFERENT IMMUNE 
CELLS 

 
Leucocytes or white blood cells are the cells 
responsible for immunity [18]. These cells have 
different actions and mechanisms from the onset 
of their activation to the consequent removal or 
destruction of the foreign invading agent [19]. 
The cells could morphologically be classified as 
granules-containing cells (granulocytes) and 
Non-granules contains cells (agranulocytes) [20]. 
Both cells depending on the invading agent 
particularly viral infections, mediate immune 
responses in various ways. 
 

Granule-containing cells including neutrophils, 
basophils and eosinophils release the content of 
their granules which are mostly hydrolytic 



 
 
 
 

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93 

 

enzymes that could easily destroy the invading 
agent [21]. 
 

The agranulocytes are do not contain granules. 
However, they are mostly capable of 
endocytosis, engulfing the invading agent and or 
its antigen there by causing its destruction [22]. 
Similarly, these cells including macrophages, 
monocytes, dendritic cells, natural killer cells, 
mast cells are also capable of releasing 
cytokines, interleukins and interferons which also 
cause the death and destruction of the invading 
agents [23]. These chemicals also play critical 
roles in B cells activation proliferation leading to 
secretion of different immunoglobulins [24]. 

 

3. ANTIVIRAL IMMUNE RESPONSES 
 

Infections of viruses usually differ with other 
invading agents particularly in its mechanism and 
responses [24]. Retro viruses are able to enter 
into cells and utilize the cellular machinery to 
replicate its genome which at the final end will 
cause the destruction of the host cell [25]. 
Although there are systems that facilitate cellular 
recognition upon entry of invading foreign 
agents, viruses lack these specialized signals 
such as Pathogen associated molecular patterns 
(PAMPs) [26]. They could only be recognized 
with interaction of Toll-like receptors (TLRs)         
with their nucleic acids [27]. These interactions

.  
 

Fig. 1. Description of immune system and activation of antiviral immune response 
 



 
 
 
 

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between Toll-like receptors and the viral nucleic 
acids initiates a positive immune response via 
the release of interferons consequently mediating 
a B-cell mediated immunity with the concomitant 
production of Antibodies [26]. 
 
Viral infections have been associated with the 
type of the hosting system and nature of organs. 
Principally the nature of infection and mode of 
immune response could influence the 
pathogenesis of the disease [28]. Considering 
the respiratory system, it comprises the airways 
which are formed by a layer of epithelial cells 
which in essence is part of the innate immunity. 
Mucosal secretions by the epithelial wall serve 
also as part of the innate immunity. However, 
with a lot of viral population being part of the host 
microbiome particularly in the respiratory system, 
it may affect a possible antiviral immune 
response [29]. Similarly, various modifications 
during leucocytes differentiation might allow for 
lack of responses against the viral population in 
the microbiome. With that said however, no 
available studies have shown direct relation 
between onset of viral immune response and the 
microbiome in respiratory tract [30]. 

 
4. CORONA VIRUSES 
 
Coronaviruses are members of a large family of 
viruses causing illnesses associated with 
respiratory tract. These viruses belonging 
collectively to the order Nidovirales, are positively 
stranded RNA viruses [31]. 
 
The coronavirinae are further subdivided into 
alpha, beta and gamma subfamilies each 
representing a particular nuclear configuration of 
the viral RNA [32]. The viral RNA contains a 5’ 
cap and 3’ polyA tail allowing to act as a 
messenger RNA for expression of its replication 
machinery proteins [31]. Thus a major part of the 
genome encodes for the replication machinery 
proteins hence its rapid replication upon entry 
into the host cell. Structural organization of the 
viral cell showed the virus as cylindrical with 4 
specified proteins encoded by the minor sections 
of the genome [33]. These include the membrane 
(M) protein, the Spike (S) protein, Envelop (E) 
protein and Nucleocapsid(N) protein. 
 
A major distinction is seen in the beta subfamily 
where another (5

th
) structural protein is observed, 

the Hemagglutinin esterase protein [31]. The 

protein is thought to enhance spike protein 
activity and establish interaction with sialic acids 
on glycoproteins present on the surface of host 
cells there by facilitating viral entry [34]. 
 
Upon viral entry, the expression of the replication 
machinery is achieved. The Replicase protein 
expression is achieved in a series of complex 
mechanisms starting with expression of two 
polyproteins ppla and pplb [31]. Studies showed 
distinct controlled mechanisms in expression of 
these proteins suggesting the complicated nature 
of the replication machinery expression which 
powers the virus with its rapid spread [35]. Next 
is the assembly of the viral replication complex to 
replicate the Viral RNA. 
 
The replication machinery utilizes viral RNA to 
synthesize the viral genome again. The viral 
RNA synthesis proceeds with formation of 
Genomic RNA and the sub genomic RNA which 
is concerned with expression of structural and 
accessory proteins. Their encoding genes are 
located along the 3’ terminal end representing 
nest of RNA [36]. The process is completed with 
translation of the structural proteins of the virus 
which are then transferred to the Endoplasmic 
Reticulum, assembled and further released as 
mature varions. 

 
5. COVID-19 
 
The Corona virus disease-2019 was reported to 
be caused by a new strain of SARS-CoV2 in 
December 2019 [37]. Patients have shown 
pneumonia like symptoms and others associated 
with severe respiratory syndrome [38].  
According to WHO, the massive spread of 
COVID-19 has reached more than 10 countries 
globally and could possibly infect 20 million 
people. 
 
As at March 2020, there have been 274,202 
reported cases for Covid-19 out of which 11,354 
deaths have been reported. Positively, about 
90,000 individuals have completely recovered 
and for the first time no new indigenous case has 
been recovered in the Chinese city of Wuhan 
where it started. In Nigeria, so far 135 cases 
have been confirmed with 2 deaths most of 
which have been from individuals with history of 
foreign travels [39]. Measures have already been 
in place by various government agencies to 
contain and control the spread of the virus. 

 



 
 
 
 

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Fig. 2. Summary of life cycle and pathogenesis of SARS-CoV2; the viral proteins together with 
yet to be elucidated mechanisms inhibit activation of transcriptional factors IRF3 and NFkB. 

These factors initiate a signal cascade that results into blocking of viral replication and 
assembly (adopted from [5]) 

 
Key molecular mechanisms of the SARS-CoV2 
pathogenesis are still unknown [40]. However, its 
pathophysiology involves viral entry in respiratory 
droplets  into the lungs via the airways [31]. 
Major target of the virus is the alveolar cells 
which play critical roles in gaseous exchange 
during respiration [41]. Interaction between the 
viral Spike proteins and the ACE receptor 
ensures viral entry into the alveolar cells with the 
concomitant of structural disintegration. The 
Inflammatory response initiated was due to 
release of pro-inflammatory cytokines such as IL-
6 and TNF-alpha [37]. These two cytokines 

interact with the brain’s hypothalamus resulting in 
physiological changes including increase in body 
temperature and fever. Additionally, the response 
results in vasodilation and increase vascular 
permeability. As such, with corresponding fluid 
accumulation, causing increased breathing 
capabilities and by extension breathing difficulty 
[31]. 
 

As it is currently no specified treatment or 
vaccine for Covid-19 [42]. However, various 
clinical trials have been conducted and have 
shown significant results. The United States’ 



 
 
 
 

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Food and Drug administration has shown 
promising results regarding the use of the anti-
malarial drug chloroquine and its derivative as 
possible treatment for Covid-19 [41]. However, 
the FDA is yet to give a formal approval contrary 
to previous claims. Possibly, target in 
development of treatment include study on 
molecular mechanism of the disease 
pathogenesis to target the viral key proteins [42]. 
However, as such processes could take longer 
period, the rapid spread of the disease may not 
allow for that. 
 

6. HOW DOES SARS-COV2 POSSIBLY 
EVADE ANTIVIRAL IMMUNE 
RESPONSE? 

 
The SARS-COV2 is a novel corona viral strain 
responsible for the December 2019 pandemic. 
The key mechanisms through which these 
coronaviruses including the SARS-CoV2 tries to 
circumvent immune response are still under 
investigation [36]. However, as with most 
coronaviruses, the SARS-CoV2 utilizes its 
structural proteins to gain entry into the host cell 
cytosol as well as suppress signaling pathways 
particularly with the Toll-like receptors (TLR) [31]. 
Usually, the interaction between the viral nucleic 
acid is with TLR7 and TLR3 [27]. This interaction 
initiates a signal cascade involving the 
transcriptional factors IRF3 and NFkB. 

 
These transcriptional factors are further 
translocated into the nuclei where they activate 
the machinery for expression of Pro-inflammatory 
cytokines and interferons particularly IFN1 [33]. 
IFN in turn activates the JAK-STAT pathway via 
phosphorylation of STAT-1 and -2. The combine 
activated forms of STAT-1 and -2 further form 
complexes with IRF9 with the immediate release 
of active Interferon stimulating genes (ISGs) 
resulting in a massive suppression of viral 
replication [33]. 
 

7. CONCLUSION 
 
The Covid-19 pandemic has so far reached a 
very disturbing rate. Measures have continued to 
be in place to prevent the continued spread of 
the virus, and so far there have been promising 
results. Researchers have continued to 
investigate the mechanism of antiviral response 
to the SARS-Cov2 and there have been positive 
results. Moreover, there is hope that in the near 
future, vaccine and definitive treatment to Covid-
19 will come to fruition. 

CONSENT 
 

It is not applicable. 
 

ETHICAL APPROVAL 
 

It is not applicable. 
 

COMPETING INTERESTS 
 

Authors have declared that no competing 
interests exist. 
 

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