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Virology
DEFINATION: Study of the most infectious agents.

LIVE VACCINE KILLED VIRAL VACCINE BOTH

Mumps, Measles & Rubella Hepatitis A vaccine Polio
vaccine.
Rota Virus vaccine Rabies vaccine Influenza
Yellow fever vaccine Japanese encephalitis vaccine
Adenovirus vaccine
Smallpox vaccine
Varicella vaccine (Varivax &
Zostavax)
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✓ CYTOPATHIC EFFECT➔ VISUAL OR FUNTIONAL CHANGE IN INFECTED CELLS TYPICALLY

ASSOCIATED WITH DEATH OF CELLS.
✓ TRANSMISSION FROM MOTHER TO OFFSPRING IS➔VERTICAL TRANMISSION ALL OTHERS ARE
HORIZONTAL TRANSMISSION.
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DNA virus with disease RNA virus with diesease

Paramyxovirus➔ Measles, Mumps & HSV➔Herpes
Parainfluenza
Influenza virus➔ Influenza Hepatitis D virus➔ Hepatitis D
Hepatitis A, C, D, E viruses➔ Hepatitis A,C, Cytomegalovirus➔Mononucleosis syndrome
D, E virus respectively
Rota virus➔ Rota Epstein Barr virus➔ Infectious Mononucleosis
Rubella virus➔ Rubella Varicellla Zoster virus➔ Chicken pox
HIV➔ Aids Human Papilloma Virus➔ Warts
Rabies➔ Rabies Adenovirus➔ Pharyngitis
Dengue virus➔ Dengue

UQ: Approaches to diagnose viral disease by use of any clinical specimen:

1. Identification of virus in cell culture.
2. Microscopic identification directly in the specimen.
3. Serologic procedures to detect a rise in antibody titer or presence of IgM antibody.
4. Detection of viral antigens in blood or body fluids
5. Detection of viral nucleic acids in blood or patients cells
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UQ: Virus that spread during dental treatment:

Hepatitis B virus, HIV, Influenza Virus, CMV, HSV 1 & 2, Measles, Mumps, Rubella & Adenovirus.

UQ: VERTICALLY TRANSMISSIBLE VIRUSES:

DNA Enveloped virus DNA Non-enveloped virus

1. Herpes virus 1. Adenovirus
• Herpes Simplex virus type 1 and 2
• Varicella-Zoster Virus- Chickenpox in children,
when it reoccurs it causes Shingles.
• Cytomegalovirus- Congenital malformations
• Epstein-Barr Virus- Infectious Mononucleosis
• Human Herpes virus 8- Kaposi’s sarcoma
2. Hepatitis B virus 2. Papillomavirus
3. Pox Virus 3. Parovirus
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RNA Enveloped Virus RNA Non-enveloped virus

1. Respiratory viruses: 1. Enteroviruses- infect enteric tract.
• Influenza A and B viruses • Polio virus
• Parainfluenza viruses • Coxsackie virus
• Respiratory syncytical virus • Echoviruses
• Human metapneumovirus

2. Measles, Mumps and Rubella Viruses. 2. Rhinovirueses

3. Rabies Virus- Fatal encephalitis 3. Rota virueses
4. Hepatitis C virus-Chronic hepatitis and 4. Hepatitis A virus
hepatic carcinoma
5. Human T-Cell Lymphotropic Virus-Leukemia 5. Noravirus
& autoimmune disease (Tropical spastic
paraparesis)
6. Human Immunodeficiency Virus 6. Hepevirus

HERPEVIRUSES, POXVIRUSES, HUMAN PAPILLOMA VIRUS

• Primary clinical infestation: Skin lesions.
• Herpes and Poxvirus- Linear double stranded DNA, HPV- Circular double stranded
DNA.
• Herpes and HPV- Replicate in the nucleus, Poxvirus- Replicate in cytoplasm

HERPESVIRUSES➔GIANT CELLS
Icosahedral core surrounded by a lipoprotein envelope. Genome is linear double stranded
DNA, Virion does not contain polymerase, large (120-200nm), Herpes virus replicate in the
nucleus forming intracellular inclusions ONLY virus to obtain their envelope by budding from
the nuclear membrane, Life-long latent infections and contain- Tegument- Located b/w
nucleocaspid and the envelope- Role in viral replication.

HSV type 1 and 2, VZV, CMV- INDUCE FORMATION OF MULTINUCLEATED GIANT

CELLS.
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HERPES VIRUS

ALPHA BETA GAMMA

• HSV 1 & HSV 2 • CMV • EBV
• VZV • HHV-6 • HHV-8

Infect epithelial cells Infect and become Infect and become

primarily latent infections latent in variety of latent primarily in
of the neurons tissues lymphoid cells.
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HERPES SIMPLEX VIRUSES (HSV)

HSV 1➔ABOVE WAIST LESION HSV 2➔ BELOW WAIST LESION
Life cycle Virus Binds to Cell using Nectin and VP16➔Virus Fuses With the membrane➔ Capsid enters inside the
Cell➔Now linear DNA and VP16 protein is inside the human Cell➔Linear DNA is incorporated into Cell DNA
while VP16 protein activates IE gene which form IE protein which in turn forms early protein like DNA
polymerase and Thymidine kinase➔Cell in which Virus is present may undergo Lysis by virus multiplication or
may be in latent phase (mainly HSV 1 remains latent in Trigeminal ganglion while HSV 2 in Lumbar and
sacral Ganglion) ➔Upon Any Stressful conditions Cell may enter from latent to lytic phase .
Transmission Saliva HSV 1➔ Lesion on face.
Sexual Contact HSV 2➔ Lesion in the genital area.
Pathogenesis HSV replicates in the skin & mucous membranes at the initial site of infection. Progeny virus infects adjacent
neurons and the nucleocaspid migrates up the axon by RETROGRADE axonal flow to the nucleus of the neuron➔
Viral DNA becomes a closed circular DNA➔ remains as episome DOES NOT integrate into human DNA.
Trauma or Stressful conditions like radiation➔Virus which used the anterograde mechanism to travel towards
ganglion now move back and can cause vesicular skin lesions which contains Pus having viruses + Cellular Debris
and lesions also contains Multinucleated Giant Cells .
Skin lesion progress from Erythema➔ Papules➔ ulcers➔crusts.
Prodromal itching or tingling occur.
Clinical HSV 1
Findings 1. Gingivostomatitis➔fever + Vesicular lesion in mouth of children
2. Orolabial Herpes( Herpes Labialis)➔These are Cold Sores or Fever Blisters in which vesicular lesions are
on mucocutaneous junction of lips and nose.
3. Keratoconjunctivitis➔Corneal Ulcer .If reoccur then Blindness results.
4. Encephalitis➔Involves Temporal Lobe and leads to Seizures, headache and Vomiting.
5. Herpetic Whitlow➔Lesions on fingers when contact occur with patient's lesions.
6. Herpes Gladiatorum➔Vesicular Lesions on head, trunk and neck in wrestlers and those who have close
body Contact
7. Eczema Herpeticum (Kaposi’s varicelliform eruption) ----->Infection on skin with atopic Dermatitis
mostly in children.
8. Disseminated Disease➔Pneumonia and Esophagitis
9. Erythema Multiforme➔Central Red area surrounded by normal area and then this is further surrounded by
ring of red area thus forming Target of Bull’s eye lesions

HSV 2
1. Genital Herpes➔Lesions on Genitals involving cervix and associated with fever and Lymphadenopathy.
These are more severe in primary disease rather than during recurrence.
2. Neonatal Herpes➔Occurs in neonates if during delivery comes in contact with lesions in the genitals. They
are severe if mother is infected with primary infection because in secondary infection sufficient IgG passes to
Child to protect him/her from infections. Cesarean Section on women may prevent the disease spreading to
Neonates.
3. Aseptic Meningitis
4. Erythema Multiforme
Laboratory 1. Isolation from lesion and Grow in the Cell Culture. When it shows Cytopathic Effect use ELISA or
Diagnosis Fluorescent Antibody Staining to identify Virus. In ELISA use Monoclonal Antibody against GpG to
distinguish HSV 1 from HSV 2.
2. Stain Cells from Base of Lesions with Giemsa Stain(Tzanck Smear) and detection of
3. Multinucleated Giant Cell➔ Presumptive
4. PCR on Spinal Fluid In case of Encephalitis. More sensitive and rapid then culture.
5. Serological Test➔For Primary Infection
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VARICELLA ZOSTER VIRUS➔GIANT CELLS+

VESICULAR RASH+ SHINGLES, SENSORY ROOT
AFFECTED. CUTANEOUS SCARRING IN
DERMATOMAL PATTERN.

Life Cycle Similar to HSV.

Transmission Respiratory Droplets
Direct contact with the lesions
Pathogenesis Virus infects mucosa of upper Respiratory Tract➔Enters Blood➔Reaches to skin➔Cause Lesions Virus
Affects Sensory Ganglion➔Uses Retrograde axonal Transport Mechanism➔Become Latent in Dorsal Root
Ganglion (in Nucleus not integrated into Cellular DNA)➔When Activated➔Cause Vesicular Skin Lesions
and Nerve Pain of Zoster.
Clinical Findings Incubation period 14-21 days.
Varicella: Mild in children but severe in adults.
1. Itching Pruritus- Prominent symptom.
2. Fever
3. Malaise
4. Papulovesicular Rashes (appear in crops on the trunk and spreads to the head and extremities )
5. Reye’s syndrome in Children Taking Aspirin

Zoster:
1. Painful vesicles along course of sensory Nerve on Head or Trunk
2. It Can Cause Post Zoster neuralgia (Post herpetic Neuralgia)
3. Pneumonia in Immunocompromised
Laboratory 1. PCR tests to detect viral DNA and DFA tests on skin lesions.
diagnosis 2. In Tzanck smear➔See Multinucleated Giants Cells➔Presumptive
3. Identification in specific antiserum after isolation in Cell Culture ➔Definitive Diagnosis➔4 fold Rise in
antibody titer is diagnostic for Varicella
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CYTOMEGALOVIRUS➔BLUEBERRY MUFFIN
RASH+OWL’S EYE INCLUSION BODIES
Lifecycle Same as HSV.
Transmission Saliva, Breast Milk, Birth Canal, Placenta Blood, Transfusion and Organ Transplant
Pathogenesis 1. Cytomegalic inclusion disease in Fetus in which there are multinucleated giant Cells with
prominent intranuclear inclusions.
2. Congenital Abnormalities in fetus are more severe when fetus is affected during first
trimester when his organogenesis is occurring.
3. Latent in Monocytes, Kidney and Cervical Cells and reactivated when Cell mediated immunity
is Less.
Clinical Findings • Cytomegalic Inclusion disease➔ Microcephaly, Seizures, Deafness, Jaundice and
Purpura(Resembles with Blueberry muffins)
• Hepatosplenomegaly
• Mental RetardatioN➔ Cytomegalic inclusion
• Heterophil-Negative mononucleosis in immunocompetent➔Fever,lethargy and abnormal
lymphocytes in peripheral blood smears
• Pneumonitis
• Esophagitis Immunocompromised patients
• Hepatitis
• Irritable colitis with diarrhea and also rhinitis in AIDS patient
• CMV is excreted in urine of infected infant.
Laboratory • Culture in Special Tubes(Shell vials)+ Use Immunofluorescent antibody ➔ Diagnosis within 3
Findings days
• For Finding Drug Resistance to Ganciclovir ➔Use Culture.
• Oval owl’s eye shaped intranuclear inclusion bodies in urine or tissue using
histological and fluorescent antibody staining A 4 fold Rise in Antibody Titer ➔Diagnostic
• PCR for CMV DNA or viral mRNA in tissue or body fluids such as spinal fluid & amniotic fluid
are often used.
• Detect pp65 (Antigen in nucleocapsid) within blood lymphocytes using Immunofluorescence
assay.
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EPSTEIN-BARR VIRUS
(EBV)➔LYMPHOMAS+WHITE PLAQUES ON
LATERAL ASPECT OF TONGUE.
It Contains: - Viral Capsid Antigen (VCA), Early Antigen, Epstein-Barr nuclear antigen, Lymphocyte-
determined membrane antigen, Viral Membrane Antigen (Neutralizing activity is directed against this
antigen)
Life cycle Similar to HSV .It infects B lymphocytes for C3 complement receptor site.
Transmission Saliva e.g. During Kissing
Pathogenesis 1. Infects Oropharynx➔Spreads to Blood ➔Enters the B Cell➔Remains Latent within B Cell
2. CD8+ cells (Atypical Lymphs) React against these B Cells IgM forms Against VCA➔ IgG
forms against VCA and persist for Life.
3. Nonspecific Heterophile antibodies are present.(nonspecific Because Also present in
individual with Hep. b and Serum Sickness)
“Heterophils are those antibodies which are detected by tests using antigen different from
antigens that induced them and it seems EBV modifies Cell membrane Constituents in such a
way that it becomes antigenic and induces heterophil antibodies. They Disappear within 6
months after Recovery.”
Clinical • Infectious Mononucleosis➔Fever+ Sore Throat + Lymphadenopathy + Splenomegaly
Findings (May Rupture) +Encephalitis (some patients), Anorexia and Lethargy (prominent).
• X-Linked Lymphoproliferative Syndrome- Severe often fatal, progressive form that occurs
in children with an inherited immunodeficiency.
• Hairy Leukoplakia➔Whitish nonmalignant lesions with irregular hairy surface on lateral
Side of Tongue.
• It is associated with Burkitt’s lymphoma (by Mutating c-myc proto-oncogene) ,Hodgkin's
Lymphoma and Nasopharyngeal Carcinoma.
• Post-transplant lymphoma most common B cell lymphoma occurs in both bone marrow
and solid organ transplanted patients. Reduction in degree of immunosuppression causes
all lymphomas to regress.
Laboratory A-HEMATOLOGIC APPROACH
Diagnosis Smear Shows enlarged atypical lymph with expanded nucleus and Vacuolated Cytoplasm.
B-IMMUNOLOGIC APPROACH
• Heterophil antibody test for early Diagnosis but not for prior infection.
• Monospot test to detect heterophile antibody. (No longer recommended produces false
positive test)
• EBV-specific Antibody Test. Primarily in diagnostically difficult cases. The IgM VCA
antibody response used to detect early illness while IgG VCA antibody response shows
prior infection.
• Detection by fluorescent antibody staining of nuclear antigen in cord lymphocytes

HUMAN HERPES 8➔ KAPOSI’S SARCOMA

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POX VIRUSES: SMALLPOX VIRUS➔ERADICATED

Lifecycle Penetration of the cell & uncoating➔ Virion DNA-dependent RNA polymerase synthesizes
early mRNA➔Translated to early, non-structural proteins➔Viral DNA is replicated➔Late
structural proteins are formed that will form progeny virions.

All steps occurring in the cytoplasm.

Transmission Respiratory aerosol
Direct Contact
Pathogenesis INCUBATION PERIOD
Virus infects the upper respiratory tract & local lymph nodes➔ enters blood (Primary
viremia)➔Internal organs are infected the virus reenters the blood (secondary viremia) &
spreads to the skin.
Rash results from viral replication in the skin➔Followed by damage caused by cytotoxic T
cells attacking virus infected cells.
Clinical Findings Incubation period 7-14 days.
Sudden onset of prodromal symtoms➔ Fever &malaise followed by rash which is worse on
the face and extremities than on the trunk.
Rash➔Macules➔Papules➔Vesicles➔Pustules➔Crusts in 2-3 weeks.
Laboratory Growing virus in cell cultures
Findings Chick embryos
Detecting viral antigens in vesicular fluid by immunofluroscence.
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HUMAN PAPILLOMAVIRUS (HPV)➔

WARTS+RAISED DRY VERRUCUOS LESIONS
Non-enveloped viruses with double stranded circular DNA & Icosahedral nucleocaspid. HPV genome has
seven early genes (E1-E7), E6 and E7 are implicated in carcinogenesis.

Life cycle After attachment & uncoating genome DNA moves to the nucleus➔mRNA synthesized by host
cell RNA polymerase➔Initial progeny genomes are maintained as episomes in the nucleus. Most
of the synthesis of progeny viral DNA occurs in conjunction with cellular DNA synthesis during
S phase➔ Late mRNA encode both L1 and L2. L (contains HPV virions) & L2 (Aids in
packaging of the genome DNA into progeny virions as well as uncoating the genome when they
infect the next cell).
In human tissues initially infect the basal but no virus is produced by the virus.
Infectious virus particles are found in terminally differentiated squamous cells rather than in basal
cells.
In malignant cells, viral DNA is integrated into the host cell DNA in the vicinity of cellular proto-
oncogenes & E6 & E7 are overexpressed.
Transmission Skin-to-skin contact, including genital contact.
Micro-abrasions in the skin allow access to the basal epithelial cells.
Genital warts most commonly transmitted.
Skin warts common in children and young adults & tend to regress in older adults.
HPV from mother to neonate in child birth➔ warts in mouth & in respiratory tract, especially on
the larynx, of the infant.
Pathogenesis Infect the squamous cells produce➔ Perinuclear cytoplasmic vacuole➔Called KOLIOCYTES
(Hallmark)

Clinical Findings Skin & Plantar warts➔HPV 1-HPV 4.

Genital warts (Condylomata acuminata)➔HPV-6 &HPV-11
HPV-6 AND HPV-11➔ Respiratory tract papilloma, especially laryngeal papillomas in young
children
HPV-16 & HPV-18➔ Carcinomas of the cervix, penis & anus as well as premalignant leisions
called Intraepithelial neoplasia.
Laboratory Presence of Koilocytes in the lesions.
Diagnosis PCR for detection of DNA of 14 high risk genotypes
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REPIRATORY VIRUSES

ORTHOMYXOVIRUSES PARAMYXOVIRUS CORONAVIRUS

Influenza Virus • Measles

• Mumps
• Respiratory syncytial virus
• Parainfluenza virus

HUMAN INFLUENZA VIRUS

• A➔ Worldwide epidemics B➔ Major Outbreaks of influenza. C➔ Mild respiratory tract
infections.
• Segmented single strand RNA genome, a helical nucleocaspid & outer lipoprotein envelope. Virion contains
RNA=dependent RNA polymerase➔Transcribes negative polarity.
• Envelope contains 2 different types of spikes➔ NEURAMINIDASE➔Cleaves Neuraminic acid
(sialic acid) to release progeny virus from the infected cell. It also degrades the protective layer of the of mucus
in respiratory tract➔enhances the ability of virus to gain access to the respiratory epithelial cells.
• HEMAGGLUTININ➔ Bind to cell surface receptor (neraminic acid, sialic acid) to initiate the infection of
the cell.
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• In clinical laboratory Hemagglutinin➔ Agglutinates the RBC➔ Basis of the diagnostic test called
Hemagglutination inhibition test.
• Influeza virus especially Influeza A, shows changes in the antigenicity of their hemagglutinin and
neuraminidase.
1. Antigenic shift: Major change based on reeassortment of the
segments of the genome RNA. In reassortment entire segments of
RNA are exchanged, each one codes for a single protein e.g.
Hemagglutinin.
2. Antigenic Drift: Minor change based on mutations in genome RNA.
Influeza A virus➔ 2 matrix proteins. M1➔located b/w internal
nucleoprotein and the envelope & provides structural integrity.

M2➔ Forms an ion channel b/w internal of the virus & external milieu,
plays an important role in uncoating of the virion after it enters the cell.

Influenza viruses have group-specific and type-specific antigens.

➔Internal Ribonucleoprotein in the nucleocaspid is group-specific

antigen that distinguishes influenza A,B & C viruses.

➔Hemagglutinin & Neuraminidase are the type specific antigens

located on the surface.

Pathogenesis • Inflammation of the mucosa of the upper respiratory tract such as the nose & pharynx and lower
respiratory tract such as the larynx, trachea and bronchi. Pneumonia which involves the alveoli may also
occur.
• After the virus has been inhaled➔ Neuraminidase degrades the protective layer mucus layer of the
respiratory tract➔allowing the virus to gain access to the cells of the upper & lower respiratory tract.
Virus restricted to this layer as the protease that cleave hemagglutinin are only found in the respiratory
tract.
• Severe myalgias➔circulating cytokines.
• Necrosis of the superficial layer of the respiratory epithelium.
• Influenza virus pneumonia➔Interstitial in location.
Clinical Incubation period 24-48h.
Findings Fever, myalgias, sore throat and headache develop suddenly.
Symptoms resolved within 4 to 7 days, but influenzal or bacterial pneumonia may complicate the course.
Reye’s syndrome.
Lab Diagnosis • PCR based tests that detect influenza virus RNA in respiratory specimens.
• Nucleic acid amplification tests have high specificity and acceptable specificity
• ELISA for viral antigen in respiratory secretions such as nasal or throat washings, nasal or throat swabs,
or sputum.
• Detection of antibodies in patient’s serum.
Transmission Airborne respiratory droplets.
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RESPIRATORY SYNCYTIAL
VIRUS➔Bronchiolitis, Pneumonia
Surface spikes are fusions proteins➔ cause cells to fuse, forming multinucleated giant cells
(Syncytia)
Transmission Respiratory droplets
Direct contact of hands with nose or mouth.
Pathogenesis RSV infection in infants is more severe and more often involves the lower respiratory tract
than in older children and adults. Infection localized with the respiratory tract.
Severe disease in infants may have an immunopathogenic mechanism➔ Maternal antibody
passed to the infant may react with the virus➔ forming an immune complex➔ damaging
the respiratory tract cells.
Clinical Findings Infants➔ Lower respiratory tract disease such as bronchiolitis & Pneumonia.
Young children➔ Otitis media.
Laboratory Diagnosis PCR-based assay- RNA of RSV in respiratory tract specimens.
Enzyme immunoassay (Rapid antigen test)➔ detects the presence of RSV antigens in
respiratory secretions.
Immunofluorescence- Presence of virus on smears of respiratory epithelium by isolation in
cell culture.

CORONA VIRUS➔SARS
Coronavirus has a nonsegmented, single stranded, positive-polarity RNA genome. Enveloped virus with
helical nucleocaspid. No virion polymerase. Electron microscope➔ prominent club shaped in from of corona
(halo) can be seen.

Life cycle Virus adsorbs to cells via its surface spikes (hemagglutinin) after which it enters the
cytoplasm, where it’s uncoated➔Positive-strand genome is translated into 2 large
polypeptides➔Two of these peptides aggregate to form the RNA polymerase that replicates
the genome➔mRNA are synthesized & translated into structural proteins➔Assembled &
obtains it’s envelope from the ER➔Replication occurs in cytoplasm.
Transmission Respiratory aerosol
Pathogenesis Limited to the mucosal cells of the respiratory tract. 50% infections are asymptomatic.
Pneumonia➔Diffuse Edema resulting in hypoxia.
Binding of the virus to ACE-2 on surface of respiratory tract epithelium➔ contribute to the
dysregulation of fluid balance that causes edema in alveolar space.
Clinical Findings Incubation period 2-10 days.
Common Cold➔ Coryza (rhinorrhea, runny nose), scratchy throat & Low grade fever.
SARS➔ Severe atypical pneumonia➔Fever, Chills, Rigors, Malaise & Headache
Chest X-ray➔ Ground glass infiltrates that do not cavitate.
Leukopenia &Thrombocytopenia seen.
Laboratory PCR based test➔ Coronavirus RNA in blood or respiratory specimen.
Diagnosis Antibody based test.
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RHINOVIRUS➔Common cold.
More than 100 serological types, Replicate better at 33 degree Celsius than 37 degrees. Acid-labile.
Transmission Direct➔ aerosols of respiratory droplets
Indirect➔Respiratory droplets deposited on hands or on a surface then transported by fingers to nose
or eyes.
Pathogenesis Portal of entry➔Upper respiratory Tract & infection is limited to that region.
Clinical Findings Incubation period 2-4 days
Sneezing, nasal discharge, sore throat, cough & headache are common.
Illness lasts about 1 week.
Laboratory PCR based assay➔ Detecting RNA of rhinovirus in respiratory tract specimens.
Diagnosis

ADENOVIRUS➔PINK EYE
Non-enveloped viruses with double stranded linear DNA and icosahedral nucleocaspid. ONLY
virus with fiber protruding from each of the 12 vertices of the capsid. The fiber is the organ of
attachment and is a hemagglutinin.
Transmission Aerosol droplet.
Fecal oral route
Direct inoculation of conjunctivas by tonometer or fingers.
Pathogenesis Infects the mucosal epithelium of several organs (e.g. Respiratory tract both upper & lower,
GIT & the Conjunctivas)
Also causes a latent infection, particularly in the adenoidal & tonsillar tissues of the throat.
Clinical Findings Upper respiratory tract➔ Pharyngitis, pharyngoconjunctival fever & acute respiratory
disease (sore throat, fever, coryza & conjunctivitis).
Lower respiratory tract➔ Bronchitis & atypical pneumonia.
Hemorrhagic cystitis➔ Hematuria & Dysuria.
Gastroenteritis with non-bloody diarrhea➔ In children younger than 2 years of age.
Most infections usually resolve spontaneously.
Half of all adenovirus infections are asymptomatic
Laboratory Findings PCR based assay➔ DNA of the adenovirus in respiratory tract specimens.
Cell culture and detected by fluorescent antibody technique.
4 fold or greater increase in antibody titer.
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CHILDHOOD VIRUSES
MEASLES+ MUMPS➔PARAMYXOVIRUSES
MEASLES MUMPS
Diease Characterized by Maculopapular rash Characterized by swelling of the salivary gland.
in childhood.
Tranmission Respiratory Droplet Respiratory droplet.
Pathogenesis • After infecting the cells in the upper After infecting tehcells lining the upper respiratory
respiratory tract➔ enter blood & infects tract➔Virus enters the blood & infects the parotid
reticuloendothelial cells where it replicates gland, testes, ovaries & pancreas.
again➔ spread via blood to the skin. Lifelong immunity occurs in individual who have
• Rash is primarily caused by the Cytotoxic T had the disease.
cells attacking measles virus. After the rash
appears, virus cannot be recovered and
cannot be transmitted to other.
• Multinucleated giant cells which form➔
As a result of the fusion protein in the
spikes.
• Lifelong immunity
• Infection with measles can transiently
depress cell mediated immunity.
Clinical Findings Incubation period 10 -14 days. Incubation period 18-21 days.
Prodromal Phase: Prodromal phase: Fever, malaise, anorexia➔ tender
Fever, conjunctivitis (causing photophobia), swelling the salivary glands, either unilateral or
running nose & coughing occurs. bilateral.
Kopik’s spots➔Diagnostic appear
Post pubertal males➔ Orchitis (inflammation of
several days before the rash➔ they are
testicles) which if bilateral➔ Sterility.
bright red lesions with a white, central dot
that are located on the buccal mucosa.
Meningitis➔ Benign, self-limited & without
Few days later Maculopapapular rash
sequelae.
appears on the face and proceeds gradually
down the body to the lower extremities
including the palm and soles.
Measles in pregnant women➔ Increased
risk of still birth rather than congenital
abnormalities.
Labortary Findings PCR➔ For measles RNA virus PCR➔ For mumps RNA
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RUBELLA VIRUS➔ TOGAVIRUS

Baby is infected during 1st trimester of pregnancy &
confluent maculopapular rash.
One piece of single stranded RNA, an icosahedral nucleocaspid and a lipoprotein envelope. Positive
strand RNA. Surface spikes contain Hemagglutinin.
Transmission Respiratory droplets
Transplacentally from mother to fetus
Pathogenesis Initial replication of the virus occurs in the nasopharynx and local lymph nodes➔ spreads
via blood to the internal organs and the skin
Lifelong immunity.
Clinical Findings Incubation period 14- 21 days
Brief prodromal period: Fever and malaise followed by maculopapapular rash which starts
on the face then progresses downwards to involve the extremities.
Posterior auricular lymphadenopathy➔ Characteristic.
Rash typically lasts for 3 days.
Rubella in adults especially in women can cause➔ Polyarthritis.

Congenital Rubella syndrome:

Nonimmune pregnant woman effected during 1st trimester➔several significant
malformations can occur due to maternal viremia & fetal infections.
Malformations are widespread involve mainly the heart & brain.
Congenitally infected infants also have significant IgG and IgM titers long after the maternal
antibody has disappeared.

Laboratory Findings PCR based assay➔ RNAof the virus in adult or newborm specimens or in amniotic fluid.
Antibody titer 4 fold increase.
IgM➔ Indicates recent infection.
IgG➔Indicates immunity and consequent protection of the fetus.
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PARVOVIRUS B19➔Slapped cheek syndrome.

Very small non-enveloped virus with single stranded DNA genome. Negative-strand DNA (haipin
loops at both ends).
Transmission Primarily➔ Respiratory route.
Tranplacental transmission.
Blood donated tranmissions.
Pathogenesis Infects the red blood cell precursors (erythroblasts) in bone marrow➔ Aplastic Anemia
Endothelial cells in the blood vessel➔ ERYTHEMA INFECTIOSUM.
Immune complexes composed of virus and IgG or IgM also contribute to the pathogenesis
of the virus and arthritis in some adults infected with B 19 virus.
Hydrops fetalis➔ Massive edema of the fetus secondary to congestive heart failure.

Clinical Findings ERYTHEMA INFECTIOSUM (Slapped cheek syndrome, Fifth diesease)

Bright red rash that is most prominent on the cheeks, accompanied by low grade fever,
runny nose and sore throat.
“LACY”➔ Less intense, erythematous rash appears on the body

Aplastic Anemia
Children with chronic anemia, such as thalassemia, sickle cell anemia and spherocytosis
can have transient but severe aplastic anemia (aplastic crisis) when infected with B19
virus.

Fetal infections
1st trimester➔ Fetal death.
2nd trimester➔ Hydrops fetalis.

Arthritis
Small joints of the hands and feet bilaterally.

Chronic B19 infections➔ People with immunodeficiency, especially HIV- infected,

chemotherapy or transplant patients can have chronic anemia, leukopenia, or
thrombocytopenia
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Laboratory Diagnosis IgM antibodies to Parovirus B 19

Immunocompromised➔ PCR➔ Viral DNA in the blood

VIRUSES➔ INFECTING ENTERIC TRACT

Naked nucleocaspid viruses. Enterovirus within Picornavirus. Noravirus + Rotavirus➔ Diarrheal
disease. Poliovirus+ Coxsackie virus+ Echovirus+ Enterovirus➔Diesease outside the enteric tract.

POLIO VIRUS➔Paralysis
Non-segmented, single stranded, Positive polarity RNA genome, Non-enveloped virus with
icosahedral nucleocaspid. No polymerase within the virion.
Transmission Fecal-oral route➔Replicates in Intestinal tract & Oropharynx
Pathogenesis After the replication in Oropharynx & Intestine, especially in the lymphoid tissue➔ Spreads
through bloodstream into the CNS, it can also spreads retrograde along the nerve axons.
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In CNS➔ poliovirus preferentially replicates in the motor neurons located in the anterior horn of
the spinal cord➔ Death of these cells results in paralysis of the muscles innervated by these
neurons.
Virus also infects the brainstem leading to “Bulbar poliomyelitis” (with repiratory paralysis )
but rarely damages the cerebral cortex.
In infected individuals, the immune respons consists of both intestinal IgA & humoral IgG
to the specific serotype.
Infection provides life-long immunity.
Clinical Incubation period➔ 10-14 days.
Findings o Inapparent assymtomatic infection
o Abortive poliomyelitis➔ Most common; Mild, febrile illness characterized by headache,
sorethroat, nausea & vomiting.
o Nonparalytic poliomyelitis➔ Aseptic meningitis with fever, headache and stiff neck
o Paralytic poliomyelitis➔ flaccid paralysis is predominant finding, but brainstem
involvement can lead to life threatening respiratory paralysis.
Postpolio syndrome➔ Many years after the acute illness has been transcribed➔ Marked
deterioration of the residual function of the affected muscles occur many years after the acute
phase.

Laboratory Isolation of the virus or by the rise of the antibody titer.

Diagnosis Virus can be recovered from the throat, stool or spinal fluid➔ Inoculation of the cell cultures.
Virus causes a Cytopathic effect which can be identified by neutralization of CPE with specific
antisera.
PCR➔ Polio virus DNA

HEPATITIS VIRUS
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HEPATITIS A- HEPATITIS B-
Enterovirus- Hepadnavirus
Picornavirus
Important SSRNA genome DSDNA genome
Properties Non-enveloped Enveloped virion, with an
icosahedral icosahedral nucleocaspid.
nucleocaspid Envelope- surface antigen-
Replicates in the HBsAg.
cytoplasm. Core➔ DNA polymerase
Core antigen
(HBcAg)➔Located on
nucleocaspid protein form
core of virion.
E antigen (HBeAg)➔
Soluble & relased from
infected cell into the
blood➔ Imp. Indicator of
transmissibility.
Transmission Fecal-oral route o Via blood
Virus appears in the o During sexual
feces roughly 2 intercourse.
weeks before the o Perinatal
appearance of the
symptoms.
Children are most
frequently infected.
Pathogenesis UNCLEAR After infecting the
blood➔Infects the
hepatocytes & viral antigens
are displayed on the surface
of the cells➔ Cytotoxic T
cells mediate an immune
attack against the viral
antigens➔ Inflammation &
necrosis.
Pathogenesis➔CMI.
Clinical o Incubation Mean incubation period➔
Findings period 3-4 10- 12 weeks.
weeks HBV infections are
o Acute Hepatitis asymptomatic and can only
o Fever, anorexia, be detected by the presence
nausea, of antibody to HBsAg.
vomiting & Life threatening hepatitis
Jaundice- can occur.
Typical Acute infection (serum
o Dark urine, Pale sickness like
feces & elevated symptoms)➔Fever, rash
transaminase arthralgia
levels seen. Chronic➔Neuropathies,
Glomerunephristis &
Polyarteritis nodosa
(Vasculitis of small &
medium size arteries)
HEPATITIS C-Flavivirus
SSRNA, positive polarity
genome. Enveloped virion.
More than 50% of HCV➔
Chronic
infection➔Hepatocellular
carcinoma.
Blood-borne pathogen.
Infects the hepatocytes
primarily. No evidence for virus
induced cytopathic effect. Death
of the hepatocytes➔Immune
attack by cytotoxic T cells.
HCV infection➔HCC
o Acute
infection➔asymptomatic➔
o Malaise, nausea & RUQ
pain.
o Fever, anorexia, nausea,
vomiting and jaundice are
common.
o Dark urine, Pale feces &
elevated transaminase levels
seen.
o HCV➔Significant extra
hepatic autoimmune
reactions including
vasculitis, arthralgia, pupura
& Membranoproliferative
glomerulonephritis.
HEPATITIS D-
Defective virus
Can replicate only in
cells infected with
HBV b/c HDV uses
the surface antigen
of HBV (HBsAg) as
it’s envelop protein.
o Via blood
o During sexual
intercourse.
o Perinatal
Some evidence that it
maybe be cytopathic.
IgG antibody against
the delta virus is not
detected for long
periods after
infection; it is
uncertain that long
term immunity exists.
Same as HBV
Can only occur in
persons infected with
HBV.
More severe together.
Hepatitis in chronic
carriers of HBV who
become infected with
HDV is much more
sever, and incidence
of fulminant, life-
threatening hepatitis,
chronic hepatitis &
liver failure
significantly higher.
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Laboratory o Detection IgM Early Hepatitis B➔HBsAg
Diagnosis antibody & for IgM antibody to core
o 4-fold rise in antigen.(hallmark)
antibody titer. HBsAg➔ Acute infection+
Acute infection+ Prodromal
disease, Prolonged presence
indicates chronic
state+Carcinoma+ carrier.
Window Phase➔HBsAb
not detctbale and HBsAg has
disappeared. At this time
HBcAb always positive.
o Essential cause of
Cryoglobulinemia
ELISA➔Detection of Delta antigen or IgM
antibodies to HCV. If the test antibody to delta
is positive PCR➔ Detects the antigen in patient’s
presence of viral RNA in the serum.
serum should be preformed to
determine whether active HDV RNA➔Blood.
disease exists.

HEPATITIS E
o Transmission➔Fecal-oral route➔More common
than HAV in many developing countries.
o Clinically resembles hepatitis A➔ High mortality
rate in pregnant woman.
HEPATITIS G
o Transmission➔ Sexual intercourse+ blood
o Member of the flavivirus
o Chronic infection lasting for decades.

o Chronic infection➔ chronic hepatitis+ Cirrhosis.

o Diagnosis➔ IgM antibody to HEV