INTRODUCTION
The SARS-CoV-2 virus, originating from Wuhan, China since December 2019,
causing a worldwide pandemic is a positive-sense single-stranded RNA
virus (1, 2). The disease caused was called Coronavirus disease 2019
(COVID-19).
COVID-19 disease can progress mildly (81%), moderate to severe (14%)
according to pulmonary involvement, and critical (5%) with multiple
organ failure (3). The recent mortality rate has reached 6.3%, although
it varies with age, gender, occupational group, and the presence of
comorbidities such as diabetes, hypertension (4-6).
First-line defense against intracellular invaders such as viruses starts
with innate immune cells including monocytes, macrophages, neutrophils.
Activation of monocytes, macrophages, and bystanders, bridging dendritic
cells by pattern recognition receptors results in releasing of
proinflammatory cytokines such as IL-1, IL-18, IL-33, and IL-6. Those
cytokines activate Natural Killer (NK) cells. NK activation is critical
for viral defense because of both their cellular cytotoxic function as
well as their cytokine release in particular interferon-gamma that
activates both B and T cells (7). Adaptive activation is a requirement
for both eliminating invaders, constructing a proper immune memory, and
also for limiting innate activation. Studies in T cell and RAG-1
deficient mice demonstrated that lack of lymphocytes resulted in
cytokine storm syndrome and death (8). Crosstalk between natural and
adaptive immune systems constitutes our entire immune system, but every
fine-tuned interaction is a target point for invaders.
The vicious circle of cytokine storm syndrome and hyperinflammation seen
in COVID-19 deteriorate patients rapidly and mortality rate increases in
this group due to respiratory failure (9). One of the main reasons for
the rapid deterioration of COVID-19 patients is hyper inflammation and
cytokine storm syndrome (10, 11). Studies show that SARS-COV2
uses strategies to inhibit the interferon signaling pathway. Thus it can
be considered that it silences adaptive activation (12).
Although what is known about immune pathogenesis of the disease is very
limited, lymphopenia, the change of neutrophil/lymphocyte ratio in favor
of neutrophils, increased level of LDH, CRP and ferritin vary in
proportion with the severity of the disease and are used in the
follow-up of the disease (13-15). In the autopsies of the individuals
who died due to Covid-19, neutrophil, and monocyte/macrophage
infiltration and few helper T cells were detected in their lungs (16,
17). It is noteworthy that the natural killer (NK) and
CD8+ cytotoxic T cells, which are of primary
importance in the fight against viral infection, are not present in the
field (18).
Immune profiles of individuals with Covid-19 disease should be examined
and be informed more to establish explanatory immune hypotheses on this
disease. In this cross-sectional study, we aimed to investigate
peripheral innate and adaptive cells, burst and phagocytosis functions
of monocyte and neutrophils and lymphocyte apoptosis of patients with
COVID-19, We also examined any association of these immune parameters
with severity of the disease. The data compared against the normal
values of the individuals used as a healthy control group in previous
studies of the group or the defined normal values of the subgroups.
Delineation of the phenotypic and functional impairments created by the
SARS-CoV-2 virus in the cells of the innate and adaptive immune systems
will help to better recognize the virus and develop treatment and
prevention strategies.