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CLINICAL AND PATHOGENETIC ASPECTS OF INFECTIOUS
MONONUCLEOSIS
Gubaidulina Gulmira Rifkatovna Bukhara State Medical Institute named
after Abu Ali ibn Sina , Uzbekistan, Bukhara, A. Navoi St. 1 Phone number: +998
Summary : For many physicians, the terms Epstein-Barr virus and infectious
mononucleosis are synonymous. Epstein-Barr virus causes approximately 90% of
infectious mononucleosis cases, with the remainder being caused primarily by
cytomegalovirus, human herpes virus type 6, toxoplasmosis, HIV infection, and
adenovirus.
The aim
is to analyze the pathogenetic, clinical and epidemiological features
of infectious mononucleosis of Epstein-Barr viral etiology, as well as problems of
diagnosis and treatment.
Material and methods.
The article presents a review of domestic and foreign
literature data on infectious mononucleosis of Epstein-Barr viral etiology. Results and
their discussion. Due to a significant increase in the incidence of infectious
mononucleosis caused by the Epstein-Barr virus, in recent years, the improvement of
methods of specific diagnostics and antiviral therapy will allow us to successfully
solve the problem of stopping the pathological process in the early stages of the
disease. But the problem of protracted forms of the disease requires a more in-depth
study.
Conclusions.
The key to success in the treatment of patients with infectious
mononucleosis is timely diagnosis, correct and strictly individual approach to both
etiotropic and pathogenetic therapy, as well as timely hospitalization of patients with
severe forms of infectious mononucleosis.
Key words:
infectious mononucleosis, Epstein-Barr virus, hepatitis
Abstract.
Epstein – Barr virus and infectious mononucleosis are synonymous
for many physicians. Epstein – Barr virus causes approximately 90% of cases of
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infectious mononucleosis, while the rest of the cases are associated mainly with
cytomegalovirus, human herpesvirus type 6, toxoplasmosis, HIV infection and
adenovirus. Aim. Pathogenetic, clinical and epidemiological features of Epstein –
Barr virus infectious mononucleosis have been analyzed as well as the problems of
its diagnosis and treatment.
Materials and methods.
The article presents an overview of Russian and
foreign literature data on Epstein – Barr virus infectious mononucleosis. Results and
discussion. In connection with a significant increase in the incidence of infectious
mononucleosis caused by Epstein – Barr virus in recent years, improvement of
specific diagnostic methods and antiviral therapy will successfully solve the problem
of arresting pathological process at the early stages of the disease. However, the
problem of chronic forms of the disease requires in-depth study.
Conclusion.
The key to success in treatment of patients with infectious
mononucleosis is timely diagnosis, correct individual approach to etiotropic and
pathogenetic therapy, as well as timely hospitalization of patients with severe forms
of infectious mononucleosis.
Key words:
infectious mononucleosis; Epstein – Barr virus; hepatitis.
The relevance of studying infectious mononucleosis (IMN) is due to the high
circulation of the pathogen among the population, the specific tropism of the herpes
virus to immunocompetent cells, lifelong persistence of the virus in the div and often
a latent course [1]. More than 95% of people worldwide are infected with the Epstein-
Barr virus, mainly in the higher socio-economic groups of industrialized countries,
primarily becoming infected at the age of 1 to 5 years [2]. In the last 10 years, the
incidence of IMN caused by the Epstein-Barr virus has increased 5-fold not only in
adults but also in infants. This is due to both a true increase in the incidence due to
the impact of various exogenous and endogenous factors, and the improvement of
laboratory diagnostic methods for this infection [3]. Infectious mononucleosis was
first described as a generalized inflammation of the lymph nodes by the famous
Russian pediatrician N.F. Filatov in 1885. Later, descriptions of outbreaks of
glandular fever appeared, presented by K.L. Pfeiffer (1888) and N.S. Korsikov
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(1901). The first report on the characteristic hematological changes in this disease
was made by G. Turk in the Vienna Medical Society in 1907. Later, in 1909, D. Berne
noticed changes in the "white blood" in glandular fever. In the blood of these patients,
he saw an increase in the number of "small mononuclears ". In 1920, scientists from
the USA F. Evans and T. Sprunt proposed to introduce the term "infectious
mononucleosis". In 1964, M.A. Epstein and J. Barr isolated a virus from the herpes
group, which was found with great consistency in patients with infectious
mononucleosis and had a tropism for lymphoid tissue, causing blast transformation
of lymphocytes [4]. The first representative of the human γ-herpesvirus family was
the Epstein-Barr virus (EBV). It was discovered through the study of B-cell lines
obtained from patients with African Burkitt lymphoma . EBV is a representative of
oncogenic DNA-containing viruses, the capsid diameter is 120-150 nm , surrounded
by a membrane, contains lipids. During virus replication, over 70 different virus-
specific proteins are expressed. However, to date, groups of immunogenic proteins
have been identified, the determination of antibodies to which makes it possible to
differentiate the stage of infection (EA - early antigen, EBNA-1 - nuclear antigen,
VCA - capsid antigen, LMP - latent membrane protein). As soon as the virus enters
the epithelium of the mucous membrane of the oropharynx and upper respiratory tract,
infection of lymphocytes occurs. There are a number of differences in the infection
of epithelial cells and lymphocytes. In epithelial cells , complete replication of the
virus occurs with the formation of a large number of virions, epithelial cell lysosomes
, which subsequently infect neighboring cells. At the time of infection of B-
lymphocytes, virus replication occurs only in a small percentage of cells, and in the
remaining cells the virus is in a latent state. The mechanism of interaction of EBV
with B-lymphocytes has been studied most thoroughly. The supercapsid of the virus
contains glycoprotein complexes - gp350, 85, 25 and 42. The gp350 complex plays a
leading role in interaction with B-lymphocytes. Its structure is similar to the
component of the C3 dg complex , and also interacts with the CD21 molecule on the
surface of the B-lymphocyte, being a receptor for it. Interacting, adhesion of the virus
to the cell and the beginning of endocytosis occur. In order for the virus to penetrate
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the cell membrane, interaction of other glycoprotein complexes with the β-chain of
the HLA class 2 molecule is necessary. At the same time, in order for the virus to
interact with epithelial cells , the presence of gp85, 25 is necessary, for which there is
a special receptor [5, 6, 7]. Antiviral protection of the div is carried out by
macrophages and other cells producing interferons (IFN) α, β and γ, they destroy and
block viruses. A number of interleukins (IL) [tumor necrosis factor (TNF), IL-6, etc.],
natural killers and factors form a specific immune response against a specific virus.
Cytotoxic T-lymphocytes (CTL) (CD8+ T-lymphocytes) and B-lymphocytes are
responsible for the production of specific antibodies that block viral replication and
viruses located outside the cell. In order for cells to function adequately and maintain
an immune response, the corresponding production of IFN and IL is necessary [8].
Generalization of viral infection at early stages leads to infection of T- and NK-cells
and chronic EBV infection with persistence of the virus in lymphocytes develops. The
persistence of EBV, despite its high immunogenicity , indicates the development of
special mechanisms by the virus to evade the immune response [5, 6, 7]. The signal
for the beginning of secretion of proinflammatory cytokines IL-1β, IL-6, IL-8, IL-12,
TNF-α by monocytes is contact with the pathogen. Biologically active molecules (
superoxide radicals, leukotrienes , prostaglandins) are produced and secreted during
autocrine stimulation of macrophages by cytokines. Endothelial cells of blood
vessels, on which the expression of adhesion molecules is induced, become targets of
the paracrine action of the same proinflammatory cytokines. Due to the latter, an
influx of circulating neutrophils and monocytes into the infection site is ensured. IL-
8 functions as an angiogenic factor, being an autocrine chemoattractant for endothelial
cells [9, 10]. NK cells, B lymphocytes and cytotoxic T lymphocytes are the main
effector cells. NK cells and T lymphocytes participate in the synthesis of
proinflammatory mediators and in the direct lysis of infected cells. B lymphocytes,
with the help of T helpers, produce antibodies and become specific for viral antigens
[11]. The BCRF-1 protein expressed by EBV coincides with the cytokine IL-10 in
amino acid sequence and causes its mimicry. Thus, it promotes the suppression of
INF-γ synthesis by peripheral mononuclear cells .
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Disruption of interferon formation and activation of secondary flora as a result
of the immunosuppressive action of the virus involve various organs and systems in
the process [5, 6, 7]. The epidemiological features of EBV mononucleosis are
determined, first of all, by a wide range of infection sources: patients with manifest
(including protracted and complicated variants) and asymptomatic forms, as well as
virus carriers. After an EBV infection, the patient excretes the virus with
oropharyngeal secretions for 2-18 months . There is a certain relationship between the
immune status and the excretion of EBV into the environment. Airborne transmission
is the main route of transmission, but contact-household (with the patient's saliva),
parenteral (with donor blood and transplants), and sexual transmission are also
possible. IMN most often occurs in the form of sporadic cases. Epidemic outbreaks
of the disease are possible in closed groups (in kindergartens, among students and
military personnel). The entry point for EBV infection is the epithelium of the
oropharynx, from where the virus penetrates into susceptible B-lymphocytes of the
lymphoid tissue of the pharynx. The virus can also penetrate through the
gastrointestinal tract. Surface receptors of the CD21 molecule for EBV are present on
the epithelial cells of the oropharynx and on B-lymphocytes. The virus initially
replicates in the epithelium of the mucous membrane of the mouth and nasopharynx,
then in the lymphoid formations of the pharynx and salivary gland ducts, as well as
in the epithelium of the cervix. After the introduction of the virus, severe hyperemia
and swelling of the mucous membranes of the oral cavity and nose appear. Severe
hypertrophy of the tonsil tissue and mucous membranes of the pharynx is observed.
Clinically, this is manifested by difficulty breathing through the nose and severe pain
when swallowing [12].
Infectious mononucleosis can occur in typical (acute) and atypical (latent,
asymptomatic) forms. The typical clinical picture includes febrile fever, tonsillitis,
generalized lymphadenopathy , hepatosplenomegaly , exanthema, the appearance of
atypical mononuclear cells in the blood, headache, fatigue, loss of appetite,
respiratory syndrome and myalgia [13, 14]. In atypical forms, the manifestations of
the main symptoms of the disease are less pronounced [12]. The duration of fever is
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from 10 days to 1 month or more, the severity varies from 37.5 to 40.5 ° C.
Involvement of the lymph nodes in IMN is usually symmetrical and includes the
submandibular, anterior cervical and posterior cervical groups [12]. Damage to the
oropharynx can manifest as granular pharyngitis, catarrhal, lacunar, follicular,
ulcerative necrotic tonsillitis. Acting specifically, the virus activates the bacterial
flora. Changes appear either from the first days of the disease or somewhat later – on
the 4th–6th day against the background of fever, lymphadenopathy and other
symptoms of the disease [12]. In the first days of the disease, moderate leukopenia
and neutropenia , lymphocytosis and plasma cells can be seen in the peripheral blood.
Characteristic changes in blood tests can be detected after the 5th day of the disease.
Leukocytosis up to 13×109/l ( hyperleukocytosis up to 18–20×109/l is possible),
lymphomonocytosis and the appearance of atypical mononuclear cells (10–60% and
higher) are observed. Clinical symptoms increase by the 4th–6th day, hepatosplenic
syndrome can be observed [12]. Acute hepatitis develops in approximately 50% of
patients with infectious mononucleosis, manifested by hepatomegaly (10–25%) and
increased transaminase activity. However, hepatitis also develops more frequently (in
80–90% of mononucleosis cases), as well as a more significant (10–20 times) increase
in alanine aminotransferase (ALT). Enzymatic activity increases gradually (within 1–
2 weeks from the onset of the disease), and in most patients the transaminase level
normalizes within a month in accordance with the resolution of disease symptoms.
An increase in cholestatic markers – alkaline phosphatase (ALP) levels and slight
hyperbilirubinemia – is noted in 5–10% of cases, with the development of jaundice in
approximately 45% of cases. In this case, virus-induced intrahepatic cholestasis is
indicated by an increase in the activity of ALP and lactate dehydrogenase (LDH),
often more significant than ALT and aspartate aminotransferase (AST) [15]. Another
important, but rare (0.5–3% of cases) cause of increased bilirubin may be autoimmune
hemolytic anemia. A fragment of viral origin is fixed to the erythrocyte membrane.
The resulting haptens transform the red blood cells into foreign target cells for
the immune system, which ultimately leads to hemolysis. Hemolysis occurs primarily
in the extravascular mononuclear phagocytic system of the liver and in the cells of the
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reticulohistiocytic system of the spleen. Changes in liver function tests can be
detected as early as the 5th day of the disease. Typical histological changes usually
develop between the 10th and 30th days of the disease. Pleomorphic infiltration of the
portal tracts, periportal zone and sinusoids with lymphocytes and monocytes with the
formation of lymphocytic foci is detected in the liver. Minimal swelling and
vacuolization of hepatocytes are typical. Proliferation of Kupffer cells and bile
capillary epithelium, bile stasis, as well as focal necrosis and granulomas can also be
recorded . Hepatitis in infectious mononucleosis usually occurs in accordance with
the severity of the disease. Cases of fulminant course with a fatal outcome have been
described. They were mainly due to immunosuppression : immunodeficiency in
Duncan's disease, lymphoproliferative diseases or liver transplantation (as a result of
primary EBV infection or reactivation). Like other manifestations of mononucleosis,
hepatitis is more severe in people over 30 years of age. Sometimes such patients
develop severe jaundice, fever, pain in the right hypochondrium, which may suggest
mechanical jaundice. Ascites may develop in severe hepatitis, as well as autoimmune
liver damage after EBV infection, which occurs lightning fast, accompanied by
cirrhosis, liver failure, portal hypertension. Rarely, jaundice is caused by
hemophagocytic syndrome, which sometimes develops in patients with EBV
infection. It is characterized by fever, hepatosplenomegaly , impaired synthetic
function of the liver, cytopenia and significant hyperbilirubinemia . Hemophagocytic
syndrome is a result of dysregulation of T-killers, which leads to proliferation and
activation of lymphocytes with uncontrolled hemophagocytosis and cytokine
production. In rare cases, hemophagocytic syndrome is severe and can be fatal [15].
Some patients may experience specific skin rashes. They typically appear after taking
penicillin antibiotics. Delayed-type hypersensitivity reaction causes exanthema. The
rash may vary in morphology: maculopapular, roseolous , urticarial , punctate,
hemorrhagic, petechial . It may tend to merge. Enanthems and hemorrhages can often
be seen during examination of the mucous membrane of the hard palate [16].
New studies have shown that Epstein-Barr virus can be a trigger for many
hematological and oncological diseases, such as thrombocytopenia, agranulocytosis,
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autoimmune hemolytic anemia, acute leukemia, nasopharyngeal carcinoma, Burkitt
lymphoma and Hodgkin lymphoma . Splenomegaly and splenic rupture in patients
with EBV usually manifests by the third week of the disease. Splenic rupture is a rare
but potentially fatal threat. Neurological complications include Guillain -Barré
syndrome, facial and other cranial nerve palsy, polyradiculoneuritis ,
meningoencephalitis, aseptic meningitis, transverse myelitis, peripheral neuritis,
encephalomyelitis. Other complications, which occur in less than 1% of patients
(pneumonia, pleural effusion, myocarditis, pancreatitis, glomerulonephritis, otitis,
sinusitis, formation of Stevens -Johnson syndrome as a variant of exanthema
progression), usually occur from two to four weeks after the onset of the disease and
are bacterial complications [12, 17, 18, 19, 20, 21]. Traditionally, the diagnosis of
IMN is based on clinical and hematological changes [22]. Currently, specific
diagnostics of IMN consists in determining the DNA of the pathogen by PCR and
various classes of specific antibodies by enzyme-linked immunosorbent assay
(ELISA). Epstein-Barr virus has specific antigens: early (EAD, EAR), capsid (VCA),
nuclear (ЕВNA), membrane (МА). If we know the time of appearance of a particular
antigen in the blood, we can diagnose acute, latent or chronic forms of infectious
mononucleosis caused by the Epstein-Barr virus [23, 24]. As soon as the virus enters
the div, the production of IgM and IgG antibodies against the capsid antigen (VCA)
begins. IgM are transient, and IgG antibodies persist for life. In the acute form of
IMN, early antigens appear: diffuse (EAD) antibodies disappear after 6 months , and
localized (EAR) antibodies persist for several years after IMN. Nuclear antibodies
(EBNA) are detected 1–6 months after the onset of IMN, the titer increases during
recovery. The appearance of capsid or early antibodies in the presence of nuclear
antibodies indicates reactivation of this infection [25].
The immunoblot method is also used , it allows to determine antibodies to
individual antigens of the pathogen [12]. An indirect sign of infectious mononucleosis
is an increase in the blood content of aminotransferases (ALT, AST) and organ-
specific liver enzymes (LDH'5, urokinase ) [22, 26]. Recovery occurs in 2-4 weeks ,
but lymphadenopathy , hepatosplenomegaly , and atypical mononuclear cells in the
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blood may persist , which indicates a protracted course of IMN [12]. During the acute
phase, patients are isolated, bed rest is prescribed and any physical activity is
excluded. It is necessary to adhere to a mechanically and thermally sparing diet rich
in proteins and vitamins [27]. Treatment of IMN is mainly based on symptomatic
therapy. In case of high fever, antipyretic drugs (paracetamol, ibuprofen) are
prescribed [28].
To resolve nocturnal snoring, severe nasal congestion, and in severe cases of
the disease, it is reasonable to prescribe glucocorticosteroids in a short course [29,
30]. Prescribing antihistamines is not justified because the occurrence of such a
complication as exanthema is not associated with an IgE -dependent immune
response. An increase in transaminases in IMN may be the reason for prescribing
hepatoprotectors and choleretic drugs. Etiotropic therapy with acyclic nucleosides is
theoretically justified, since the virus in the lytic cycle phase (which occurs in acute
productive infection) secretes thymidine kinase . With the help of this enzyme, acyclic
nucleosides are converted from an inactive prodrug form to an active form that
disrupts the synthesis of viral linear DNA [31]. The use of antibiotics is justified in
the case of bacterial flora layering, as well as in the development of complications.
When prescribing antibacterial drugs, preference should be given to cephalosporins
or macrolides [32, 33]. Conclusions. The key to success in the treatment of patients
with IMN is timely diagnostics, correct and strictly individual approach to both
etiotropic and pathogenetic therapy, as well as timely hospitalization of patients with
severe forms of IMN.
Transparency of the study. The study had no sponsorship. The authors are
solely responsible for providing the final version of the manuscript for publication.
Declaration of financial and other relationships. All authors participated in the
development of the concept, design of the study and in writing the manuscript. The
final version of the manuscript was approved by all authors. The authors did not
receive a fee for the study.
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