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Medical biology, microbiology,
virology, immunology department
RNA-VIRUSES:
PICORNAVIRUSES
ORTHOMYXOVIRUSES
PARAMYXOVIRUSES
DNA-VIRUSES:
HERPESVIRUSES.
ADENOVIRUSES
By as. Pyatkovskyy
Genera of Picornaviruses
Enterovirus
Polio, types 1-3
Coxsackie A ,
1-24
types
Diseases of the human (and other) alimentary
tract (e.g. polio virus)
Coxsackie B, types 1-6
Echo, types 1-34
Other enteroviruses,
types 68-71
Rhinovirus,
types 1-115
Cardiovirus
Aphthovirus
Hepatovirus
Others
Disease of the nasopharyngeal region (e.g.
common cold virus)
Murine encephalomyocarditis, Theiler's murine
encephalomyelitis virus
Foot and mouth disease in cloven footed
animals
Human hepatitis virus A
Drosophila C virus, equine rhinoviruses, cricket
paralysis virus
Pathogenesis of enterovirus infection
Replication in
oropharynx
Rhino,echo,
coxsackie,polio
Primary viremia
Secondary viremia
Target Tissue
Skin
Muscle
Brain
Meninges
Liver
Echo
Echo
Polio
Echo
Echo
Coxsackie
Coxsackie
Coxsackie
Polio
Coxsackie
A
A, B
Coxsackie
Clinical Picornavirus Syndromes
Virus
Polioviruses
(types 1-3)
Diseases (Virus Type)
Undifferentiated febrile illnesses
(types 1-
3)
Aseptic memingitis (types 1-3)
Paralisis and encephalitic
diseases
(types 1-3)
Coxsackievirus
group A
(A1-A, A-24)*
Acute hemorrhagic conjunctivitis (type 24)
Herpangina (types 2-6, 8, 10, 22)
Exanthem (types 4, 5, 6, 9, 16)
Hand-foot-mouth disease (types 5, 10, 16)
Aseptic memingitis (types 1, 2, 4-7, 9, 10, 14,
16, 22)
Paralysis and encephalitic diseases
(occasional types 4, 7, 9, 10)
Hepatitis (types 4, 9)
Virus
Diseases (Virus Type)
Upper and lower respiratory illnesses
Coxsackievirus
9, 10, 16, 21, 24)
group A (A1-A, A- (types
Lymphonodular pharyngitis (10)
24)*
Infantile diarrhea (types 18, 20, 21, 22, 24
variant)
Undifferentiated febrile illnesses
(types 1-
6)
Pleurodinia (types 1-5)
Pericarditis, myocarditis (types 1-5)
Aseptic meningitis types (1-6)
Paralysis and encephalitic diseases
(occasional types 1-5)
Severe systemic infection in infants,
meningoencephalitis and myocarditis
(types 1-5)
Upper and lower respiratory
illnesses
(types 4, 5)
Exanthem, hepatitis, diarrhea (types 5)
Virus
Echoviruses
(1-7, 9, 11,
29-33)*
Diseases (Virus Type)
Aseptic meningitis (many seroypes )
Paralysis and encephalitic diseases
(occasional types 1, 2, 4, 6, 7, 9, 11, 14-16, 18, 22,
30)
Exanthem
(types 1-9, 11, 14, 16, 18, 19, 25, 30,
32)
Hand-foot-mouth disease (19)
Pericarditis, myocarditis (types 1, 6, 9,
19,
22)
Upper and lower respiratory illnesses
(types 4, 9, 11, 20, 22, 25)
Neanatal diarrhea (types 11, 14, 18, 20, 32)
Epidemic mialgia (types 1, 6, 9)
Hepatitis (types 4, 9)
Virus
New
enteroviruses
Diseases (Virus Type)
Pneumonia and bronchiolitis
(types
68, 69)
Acute
hemorrhagic
conjunctivitis
(type 70)
Rhinoviruses
(1-115)
Hepatovirus
(Hepatitis A)
Aseptic meningitis,
meningoencephalitis
Hand-foot-mouth disease (71)
Hepatitis (type 72)
Upper and lower respiratory
illnesses (types 1-115)
Gastroenteritis and hepatitis A
* Reclassification of coxsackievirus A23 as echovirus 9, echovirus 8 as 1, echovirus 10 as
reovirus, echovirus 28 as rhinovirus type 1A, and echovirus 34 as coxsackievirus A24.
Properties of enteroviruses
Property
Enteroviruses
Size (nm)
22-30
Capsid form Icosahedral
Polypeptide VP1, VP2,
VP3, VP4
‘+’, single
RNA type
stain
Stable
Acid
Optimal
temperature for
growth(oC)
37
RNA
Properties
of enteroviruses
This genome RNA serves as an mRNA and
initiates
the
synthesis
of
virus
macromolecules.
The poliomyelitis virus has neither an outer
membrane nor lipids and is therefore not
sensitive to the effect of ether and sodium
desoxycholate.
POLIOMYELITIS
Picornavirus


3 types: Poliovirus
1,2,3
30 nm in size
Cultivation. SPE.
The poliomyelitis virus is
cultivated on kidney cells of
green African monkeys and on
diploid human cells devoid of
latent SV40 viruses.
The cytopathic effect is
attended by destruction and the
formation of granules in the
infected cells.
Pathogenesis
Source
of infection: Apparent and
subclinical patients
Incubation: is usually 7-14 days, but it may
range from 3 to 35 days.
Transmission
 Fecal
– oral route: poor hygiene,
dirty diapers (especially in day-care
settings)
 Ingestion via contaminated food
and water
 Contact with infected hands
 Inhalation of infectious aerosols
Pathogenesis
1. The mouth is the portal of entry of the
virus.
2. The virus first multiplies in the tonsils,
the lymph nodes of the neck, Peyer's patches,
and the small intestine.
3. Viremia
4. The central nervous system may then be
invaded by way of the circulating blood.
Poliovirus can spread along axons of peripheral
nerves to the central nervous system , and there
it continues to progress along the fibers of the
lower motor neurons to increasingly involve the
spinal cord or the brain. The anterior horn cells
of the spinal cord are most prominently involved.
Clinical Findings. When an individual
susceptible to infection is exposed to the
virus, one of the following responses may
occur:
 inapparent infection without symptoms
(asymptomatic illness), the minor illness –
90% infected people
 aseptic meningitis – 1%-2% of patients
with poliovirus infections,
 paralytic poliomyelitis, the major illness
0.1% to 2% of persons with poliovirus
Only about 1%
recognized clinically.
of
infections
are
Abortive Poliomyelitis. This is the
commonest form of the disease. The
patient has only the minor illness,
characterized by fever, malaise,
drowsiness, headache, nausea, vomiting,
constipation, and sore throat in various
combinations. The patient recovers in a
few days. The diagnosis of abortive
poliomyelitis can be made only when the
virus
is
isolated
or
antibody
development is measured.
Nonparalytic Poliomyelitis (Aseptic
Meningitis). In addition to the above
symptoms and signs, the patient with
the
nonparalytic
form
presents
stiffness and pain in the back and neck.
The disease lasts 2-10 days, and
recovery is rapid and complete. In a
small percentage of cases, the disease
advances to paralysis.
Paralytic Poliomyelitis. The major
illness usually follows the minor illness
described above, but it may occur
without the antecedent first phase.
The predominating complaint is flaccid
paralysis resulting from lower motor
neuron damage. The maximal recovery
usually occurs within 6 months, with
residual paralysis lasting much longer.
Child with polio sequelae
Lab Diagnosis
Definitive diagnosis is made by osolation of
the virus from stool, CFS, oropharyngeal
secretions
 Cell culture involves fibroblastic MRC-5 cells
CPE is usually evident within 36 hours
 Serotyping is based on neutralization of CPE
by standardized antisera using intersecting
pool followed by specific sera.
 ELISA
 IFA
 neutralizing Test
 CFT

Prevention
Both oral polio vaccine (OPV live,
attenuated， Sabin, 1957) and
inactivated poliovirus vaccine (IPV,
Salk, 1954) are avilable
IPV is used for adult immunization
and Immunocopromised patients
COXSACKIEVIRUSES
The coxsackieviruses comprise a large
subgroup of the enteroviruses. They
produce a variety of illnesses in human
beings, including aseptic meningitis,
herpangina, pleurodynia, hand, foot, and
mouth disease, myo- and pericarditis,
common colds, and possibly diabetes.
Coxsackieviruses have been divided
into 2 groups, A and B, having different
pathogenic potentials for mice.
Group A viruses produce widespread myositis
in the skeletal muscles of newborn mice,
resulting in flaccid paralysis without other
observable lesions.
Group B viruses may produce spasticity effect
in sucking mice, focal myositis, encephalitis,
and, most typically, necrotizing steatitis
involving mainly fetal fat lobules. Some B
strains also produce pancreatitis, myocarditis,
endocarditis, and hepatitis in both suckling and
adult mice.
Normal adult mice tolerate infections with
group B coxsackieviruses.
Herpangina: There is an abrupt onset of fever, sore
throat, anorexia, dysphagia, vomiting, or abdominal pain. The
pharynx is usually hyperaemic, and characteristic discrete
vesicles occur on the anterior pillars of the fauces, the
palate, uvula, tonsils, or tongue. The illness is self-limited
and most frequent in small children.
Exanthems – Rubelliform rashes
Hand, Foot, and Mouth Disease: The syndrome is
characterized by oral and pharyngeal ulcerations and a
vesicular rash of the palms and soles that may spread to the
arms and legs. Vesicles heal without crusting, which clinically
differentiates them from the vesicles of herpes- and poxviruses. The rare deaths are caused by pneumonia.
Hand-foot-and-mouth disease

Hand-foot-and-mouth
disease: mostly
coxackie A

fever, malaise, sore
throat, vesicles on
bucсal mucosa,
tongue, hands, feet,
buttocks

highly infectious

resolution – 1w
ECHOVIRUSES
(enteric cytopathogenic human orphan
viruses)
Not produce diseases in sucking mice,
rabbits, or monkeys. Monkey kidney and
human embryonated kidney cell culture
Aseptic meningitis, febrile illnesses with or
without rash, common colds, and acute
hemorrhagic conjunctivitis are among the
diseases caused by echoviruses.
Boston exanthem disease. Rashes are commonest
in young children.
RHINOVIRUSES
Rhinoviruses
are
isolated
commonly
from the nose and
throat
but
very
rarely from feces.
These viruses cause
upper
respiratory
tract
infections,
including
the
"common cold."
Orthomyxovirus Family
The name myxovirus was originally applied
to influenza viruses. It meant virus with an
affinity for mucins.
A model of the influenza virion
Types: A, B, C
Influenza A:
In Birds
16 H variants
9 N variants
In Humans
3 H variants
(H1, H2, and H3)
2 N variants
(N1 and N2)
Subtypes: H1N1, H2N2,H2N3
Influenza Viruses:
Antigenic Shift
Avian
Reservoir
Human
virus
Avian
virus
Other
mammals?
Swine
New
Reassorted
virus
Influenza Viruses:
Antigenic Drift

Gradual accumulation of mutations
that allow the hemagglutinin to escape
neutralizing antibodies (Point mutation
in HA gene)

Epidemic strains thought to have
changes in three or more antigenic
sites
Pathogenesis and Pathology
The virus enters the respiratory tract in airborne
droplets. Viremia is rare. Virus is present in the
nasopharynx from 1-2 days before to 1-2 days after
onset of symptoms.
Inflammation of the upper respiratory tract
causes necrosis of the ciliated and goblet cells of the
tracheal and bronchial mucosa but does not affect
the basal layer of epithelium.
Interstitial pneumonia may occur with necrosis of
bronchiolar epithelium and may be fatal. The
pneumonia is often associated with secondary
bacterial invaders: staphylococci, pneumococci,
streptococci, and Haemophilus influenzae.
Clinical Findings
The incubation period is 1 or 2 days.
Chills, malaise, fever, muscular aches,
prostration, and respiratory symptoms may
occur. The fever persists for about 3 days;
complications are not common, but
pneumonia, myocarditis, pericarditis, and
central nervous system complications occur
rarely. The latter include encephalomyelitis,
polyneuritis, Guillain-Barre syndrome, and
Reye's syndrome (see below).
Influenza Vaccines




Whole virus vaccine: inactivated virus
vaccine grown in embryonated eggs; 7090% effective in healthy persons <65 years
of age, 30-70% in persons ≥65 years
Split virus vaccine: previously associated
with fewer systemic reactions among the
elderly and children <12 years
Subunit vaccine: composed of H and N
Live, attenutated influenza virus vaccines
under development
Influenza: Chemoprophylaxis
Amantadine and rimantadine: effective
against type A, but not type B, influenza
viruses; block the M2 ion channel
 70-90% effective in preventing illness
 Administered to individuals at high risk of
complications who are vaccinated after
outbreak of infection, persons with
immune defficiency

Influenza: Chemotherapy
Amantadine (adults and children ≥ 1 year)
and rimantadine (adults)
 Zanamivir and oseltamivir:
neuraminidase inhibitors active against
both type A and B influenza viruses
 Reduce duration of illness by ~1 day when
administered within 2 days of the onset of
illness (uncomplicated influenza)

Laboratory Diagnosis
Throat washings or garglings are obtained
within 3 days after onset and should be tested at
once or stored frozen. Penicillin and streptomycin
are added to limit bacterial contamination.
For rapid detection of influenza virus in clinical
specimens, positive smears from nasal swabs may
be demonstrated by specific staining with
fluorescein-labeled antibody.
Paired sera are used to detect rises in HI, CF,
or Nt antibodies.
Family Paramyxoviridae
Genes:
Morbillivirus – measles virus,
Respirovirus – parainfluenza virus
(serotypes 1 and 3)
Rubulavirus - mumps virus,
parainfluenza virus
2, 4а, 4b),
Pneumovirus – RS-virus
(serotypes
PARAMYXOVIRUSES
pleomorphic
HN/H/G glycoprotein
SPIKES
F glycoprotein
SPIKES
helical nucleocapsid (RNA minus
NP protein)
lipid bilayer membrane
polymerase complex
M protein
STRUCTURE-PARAMYXOVIRUSES
Cell fusion. In the course of infection, paramyxo-
viruses cause cell fusion, long recognized as giant cell
formation.
MUMPS (Epidemic Parotitis)
Mumps is an acute contagious disease
characterized
by
a
nonsuppurative
enlargement of one or both of the parotid
glands, although other organs may also be
involved.
Properties of the Virus: The mumps virus
particle has the typical paramyxovirus
morphology. Typical also are the biologic
properties of hemagglutination, neuraminidase,
and hemolysin.
Epidemiology
The disease reaches its highest incidence in
children age 5-15 years, but epidemics occur
in army camps.
Humans are the only known reservoir of
virus.
The virus is transmitted by direct contact,
airborne droplets, or fomites contaminated
with saliva and, perhaps, urine. The period of
communicability is from about 4 days before
to about a week after the onset of symptoms.
Pathogenesis and Pathology
The virus travels from the mouth to the
parotid gland, where it undergoes primary
multiplication. This is followed by a generalized
viremia and localization in testes. ovaries,
pancreas, thyroid, or brain.
The ducts of the parotid glands show
desquamation
of
the
epithelium,
and
polymorphonuclear cells are present in the
lumens. There are interstitial edema and
lymphocytic infiltration.
Orchitis
PARAINFLUENZA VIRUS
The
parainfluenza
viruses
are
paramyxoviruses with morphologic and biologic
properties typical of the genus.
They grow welt in primary monkey or human
epithelial cell culture but poorly or not at all in
the embryonated egg. They produce a minimal
cytopathic effect in cell culture but are
recognized by the hemadsorption method.
Laboratory diagnosis may be made by the HI,
CF, and Nt tests.
PIV STRUCTURE
MEASLES (Rubeola)
Measles is an acute, highly infectious
disease
characterized
by
a
maculopapular
rash,
fever,
and
respiratory symptoms.
Properties of the Virus: Measles
virus is a typical paramyxovirus. It
lacks neuraminidase activity.
Measles virus
Pathogenesis and Pathology
Infection is contracted by inhalation of droplets
expelled in sneezing or coughing. Measles is spread
during the catarrhal prodromal period; they are
infectious from 1-2 days prior to the onset of symptoms
until a few days after the rash has appeared
The virus enters the respiratory tract, enters cells,
and multiplies there. During the prodrome, the virus is
present in the blood, throughout the respiratory tract,
and
in
nasopharyngeal,
tracheobronchial,
and
conjunctival secretions. It persists in the blood and
nasopharyngeal secretions for 2 days after the
appearance of the rash. Transplacental transmission of
the virus can occur.
Pathogenesis and Pathology
Koplik's spots are vesicles in the mouth formed
by focal exudations of serum and endothelial
cells, followed by focal necrosis. In the skin the
superficial capillaries of the corium are first
involved, and it is here that the rash makes its
appearance.
Generalized
lymphoid
tissue
hyperplasia occurs. Multinucleate giant cells are
found in lymph nodes, tonsils, adenoids, spleen,
appendix, and skin. In encephalomyelitis, there
are
petechial
hemorrhages,
lymphocytic
infiltration, and later, patchy demyelination in the
brain and spinal cord.
Koplik's spots
RESPIRATORY SYNCYTIAL (RS)
VIRUS
This labile paramyxovirus produces a
characteristic syncytial effect, the
fusion of cells in human cell culture. It is
the single most serious cause of
bronchiolitis and pneumonitis in infants.
Properties of the Virus: RS virus does
not hemagglutinate.
RSV- Structure
immunofluoresent stain
RSV- syncytium formation
Pathogenesis and Pathology
This disease is transmitted by coughing,
sneezing, sharing wash cloths towels and
other things with someone with RSV.
This disease is
extremely serious
when it comes to
children and infants
under the age of 3 and
elders.
This disease can result
in death.
Symptoms for this disease are: sneezing, runny
nose, sore throat, low fever, common cold
symptoms just more severe.
Treatment:
Supportive
Fluids, oxygen,
respiratory support,
bronchodilators
Antiviral Agents
Ribavirin (Virazole), a
synthetic guanosine
analogue, given as an
aerosol
RSV Bronchiolitis- clinical features
Prophylaxis
 Combination
live
virus
(measles-mumps-rubella)
vaccines
 Live attenuated measles virus vaccine
effectively prevents measles.
Properties of the Viruses:
All herpesviruses have a
core of double-stranded
DNA surrounded by a
protein coat that exhibits
icosahedral symmetry. The
nucleocapsid is surrounded
by an envelope.
Common and important herpesviruses of
humans include herpes simplex virus types
1 and 2, varicella-zoster virus, EpsteinBarr (EB) virus, and cytomegalovirus.
HERPES SIMPLEX:
Human Herpesvirus 1 (Herpes Labialis) &
Human Herpesvirus 2 (Herpes Genitalis).
Infection with herpes simplex virus may take
several clinical forms. The infection is most
often
inapparent.
The
usual
clinical
manifestation is a vesicular eruption of the skin
or mucous membranes. Infection is sometimes
seen as severe keratitis, meningoencephalitis,
and a disseminated illness of the newborn.
Cytopathic effect (infected cells develop
intranuclear acidophilic inclusion and then
undergo necrosis )
Herpes labialis
(cold sores, herpes febrilis).
This is the most common recurrent
disease produced by type 1. Clusters of
localized vesicles occur, usually at the
mucocutaneous junction of the lips. The
vesicle ruptures, leaving a painful ulcer
that heals without scarring. The lesions
may recur, repeatedly and at various
intervals of time, in the same location.
The permanent site of latent herpes
simplex virus is the trigeminal ganglion.
Herpes labialis
Keratoconjunctivitis.
The initial infection with herpesvirus
may be in the eye, producing severe
keratoconjunctivitis. Recurrent lesions
of the eye appear as dendritic keratitis
or corneal ulcers or as vesicles on the
eyelids. With recurrent keratitis, there
may be progressive involvement of the
corneal
stroma,
with
permanent
opacification and blindness.
Genital herpes (herpes progenitalis).
Genital herpes is characterized by
vesiculoulcerative lesions of the penis of
the male or the cervix, vulva, vagina, and
perineum of the female. The lesions are
more severe during primary infection and
may be associated with fever, malaise,
and inguinal lymphadenopathy.
Type 2 virus remains latent in lumbar and
sacral ganglia.
Neonatal herpes.
Herpesvirus type 2 may be transmitted
to the newborn during birth by contact
with herpetic lesions in the birth canal.
The spectrum of illness produced in the
newborn appears to vary from subclinical
or local to severe generalized disease
with a fatal outcome. Severely affected
infants who survive may have permanent
brain damage.
Laboratory Diagnosis
The virus may be isolated from herpetic lesions
(skin, cornea, or brain).
The appearance of typical cytopathic effects in
cell culture suggests the presence of herpesvirus
in 18-36 hours. Scrapings or swabs from the base
of early herpetic lesions contain multinucleated
giant cells.
Serology: The agent is then identified by
neutralization test or immunofluorescence
staining with specific antiserum. Antibodies
appear in 4-7 days; can be measured by NT, IHT,
CFT, RIA and reach a peak in 2-4 weeks.
HV, immune fluorescence test
VARICELLA-ZOSTER VIRUS
(Human Herpesvirus 3)
(Chickenpox, Herpes Zoster, Shingles, Zona)
Varicella (chickenpox) is a mild, highly infectious
disease, chiefly of children, characterized clinically
by a vesicular eruption of the skin and mucous
membranes. The causative agent is indistinguishable
from the virus of zoster.
Zoster (shingles) is a sporadic, incapacitating
disease of adults (rare in children) that is
characterized by an inflammatory reaction of the
posterior nerve roots and ganglia, accompanied by
crops of vesicles (like those of varicella) over the
skin supplied by the affected sensory nerves.
VARICELLA-ZOSTER VIRUS
(Human Herpesvirus 3)
(Chickenpox, Herpes Zoster, Shingles, Zona)
Both diseases are caused
by the same virus. Varicella
is the acute disease that
follows primary contact with
the virus, whereas zoster is
the response of the partially
immune
host
to
a
reactivation of varicella
virus present in latent form
in sensory ganglia.
Pathogenesis & Pathology.
Varicella: The route of infection is
probably the mucosa of the upper
respiratory tract. The virus probably
circulates in the blood and localizes in the
skin. Swelling of epithelial cells, ballooning
degeneration, and the accumulation of
tissue fluids result in vesicle formation. In
nuclei of infected cells, particularly in the
early stages, eosinophilic inclusion bodies
are found.
Varicella virus, pathogenesis
Varicella
Chickenpox
Pathogenesis & Pathology.
Zoster: In addition to skin lesions —
histopathologically identical with those of
varicella — there is an inflammatory reaction
of the dorsal nerve roots and sensory ganglia.
Often only a single ganglion may be involved.
As a rule, the distribution of lesions in the
skin corresponds closely to the areas of
innervation from an individual dorsal root
ganglion. There is cellular infiltration, necrosis
of nerve cells, and inflammation of the
ganglion sheath.
Zoster
Shingles
CYTOMECALOVIRUS
(Human Herpesvirus 5)
Cytomegalic inclusion disease is a generalized infection
of infants caused by intrauterine or early postnatal
infection with the cytomegaloviruses. The disease causes
severe congenital anomalies. Cytomegalovirus can be
found in the cervix of up to 10% of healthy women.
Cytomegalic inclusion disease is characterized by large
intranuclear inclusions that occur in the salivary glands,
lungs, liver, pancreas, kidneys, endocrine glands, and
occasionally, the brain. Most fatalities occur in children
under 2 years of age. Inapparent infection is common
during
childhood
and
adolescence.
Severe
cytomegalovirus infections are frequently found in adults
receiving immunosuppressive therapy.
Cytomegalovirus Inclusion Diseases.
Electron micrograph of a single animal
cell infected with the cytomegalovirus.
The intranuclear inclusion body has
a typical” owl-eyed” apearence.
Pathogenesis.
Cytomegalovirus
can
cause
persistent
infection in various tissues, including those of
the
salivary
glands,
breasts,
kidneys,
endocervix, seminal vesicles and peripheral
blood leukocytes. This persistent infection leads
to chronic viral excretion by the involved organ.
Transmission of virus is through contact with
infected secretions. The average incubation
period is four to six weeks.
It should also be noted that the kidneys of
organ donors can be a source of cytomegalovirus
for the recipient, and that peripheral blood
leukocytes have been implicated in the
transmission of cytomegalovirus via blood
transfusion.
Clinical Manifestations.
Cytomegalovirus infection can result in one of three
distinct clinical syndromes.
Congenital cytomegalovirus infection: hepatosplenomegaly, retinitis, a petechial/purpuric skin rash, and
involvement of the central nervous system (ventriculomegaly, intracranial calcifications, etc).
Mononucleosis syndrome (fever, malaise, atypical
lymphocytosis, pharyngitis and, rarely, cervical
adenopathy or hepatitis)
Third clinical entity is cytomegalovirus infection in
severely immunocompromised individuals. In these
patients,
infection
can
involve
the
lungs,
gastrointestinal tract, liver, retina, and central nervous
system
EB HERPESVIRUS
(Human Herpesvirus 4).
EB (Epstein-Barr) virus is
the causative agent of
infectious mononucleosis and
has been associated with
Burkitt's
lymphoma
and
nasopharyngeal carcinoma.
Epidemiology. Epstein-Barr virus is transmitted
by intimate contact.
Pathogenesis. Epstein-Barr virus is tropic for Blymphocytes.
Infectious
mononucleosis
Nasopharyngeal
carcinoma
Burkitt's lymphoma
Oncogenic Properties:
Herpesviruses have been linked with
malignant diseases in humans : herpes
simplex virus type 2 with cervical and
vulvar carcinoma; EB virus with Burkilt 's
lymphoma of African children and with
nasopharyngeal carcinoma.

acute respiratory disease,
pharyngoconjunctival fever,
nonstreptococcal exudative pharyngitis,
and primary atypical pneumonia
Laboratory Diagnosis.
The viruses have been recovered from throat
swabs, conjunctival swabs, rectal swabs, stools of
patients with acute pharyngitis and conjunctivitis,
and urine of patients with acute hemorrhagic
cystitis. Virus isolations from the eye are obtained
mainly from patients with conjunctivitis.
The viruses are isolated by inoculation of tissue
cultures of human cells in which characteristic
cytopathic changes are produced.
A new serotype that has not been isolated in cell
cultures can be detected by direct examination of
fecal extracts by electron microscopy or by
enzyme-linked immunosorbent assay.
Serology. In most cases, the neutralizing
antibody titer of infected persons shows a 4fold or greater rise against the type
recovered from the patient in NT.
The CF test, using the common antigen, is an
easily applied method for detecting infection
by any member of the group.
A sensitive radioimmunoassay can measure
serum antibody to type 5 fiber antigen.