DNA VIRUSES

POXVIRUSES-----------------------------------
- largest and most complex among all viruses (dsDNA)
- seen under LM (225 to 450nm long; 140 to 260 nm wide)
- first vaccine
- brick or oval shaped
- dumbbell shaped core: NA inside
- two lateral bodies
- irregular surface of the protein shell
- replicates in epidermal cells : “pocks” in skin
**TWO COURSES OF INFECTION:
- LOCALIZED: at the site of inoculation
- SYSTEMIC
* TWO SUBFAMILIES
1. Chordopoxvirinae
2. Entomonopoxvirinae

A. Physical and Chemical Properties

-survive in cold or freeze dried
-susceptible to UV and irradiation, formalin and oxidizing disinfectants
-resistant to 50% glycerol and 1% phenol
A.1. Antigenic Structure
- common NP antigen
- LS antigen
- agglutinogen Variola Vaccinia
- hemagglutinin
A.2. Cultivation and Host Range
A.2.1 Chick Embryo
- vesicular fluid to CAM VARIOLA VACCINIA
- pock formation in 48-72 hrs Pock
formation
A.2.2 Tissue Culture
Plaque
- monkey kidney, HeLa, chick embryocells
formation in
- Guarnieri bodies
tissue
cultures
A.2.3 Animals
Cytopathic
- scarification à
effect
B. VARIOLA VIRUS
- smallpox : progressive rash accompanied by fever with an incubation period of 10 to 17 days
- patient will be febrile and oral lesions will appear : INFECTIOUS STATE
- 24 to 48 hrs: faint macular rash will appear in the body and lesions will concentrate in head, limbs,
palms and soles (CENTRIFUGAL DISTRIBUTION)
- progression of macular rash (SYNCHRONOUS change) : macules at face to papules to vesicles to
pustules
Cytopathic effect?
- monkeys and humans The production of distinctive and characteristic visual
- variola major (30% fatality rate) changes in infected cells. Usually seen in cell cultures.
- variola minor (0.1% to 2% fatality rate)
*antigenically identical but different in biological characteristics ::::: alastrim smallpox

PREPARED BY: ROTHESSA CARINGAL, RMT 1

DNA VIRUSES

**ERADICATION OF SMALLPOX
- invented/ discovered by Edward Jenner
- Inoculated cowpox virus on May 14, 1796 to James Phipps and exposed him to smallpox infected
individuals
- May 8, 1980 – date when smallpox was eradicated
-Two cultures are maintained: (1) CDC in Atlanta, Georgia (2) State Center of Virology and
Biotechnology (VECTOR) in Kotsovo, Russia
C. VACCINIA
- cowpox virus, which is the agent used for smallpox vaccine
- artificial virus and safer
- rabbits, mice, monkeys, humans
D. OTHER POXVIRUS DISEASES
1. Cowpox
- zoonosis
- udder and teats of cows
- milking: hands or fingers
- rodents
2. Monkeypox
-squirrels / rodents from Africa (Gambian rats) as reservoir
- children playing with captive animals
- indistinguishable with smallpox but is less severe
- S/S: Fever and headache, lymphadenopathy and rash (macules at face to papules to vesicles to
pustules)
3. Buffalopox
-cattle TRANSMISSION DISEASE
- hands in contact with infected Smallpox Respiratory Generalized infection
animals droplets with pustular rash
4. Molluscum contagiosum Molluscum Direct contact Benign nodules
-benign epidermal tumor contagiosum
(single/small cluster of lesions) Orf Direct contact Localized papules/
- molluscum contagiosum virus vesicles
- contagious
Monkeypox Direct contact Generalized infection
- small, pink, wart-like tumors
that includes the skin
in face, arms, back,
buttocks
- children and sexually active
-(+) molluscum bodies in EM
- PCR for DNA sequences
- RFLP (restriction fragment length polymorphism)
5. Orf
- infected sheep/lambs to human transmission
- causes nodules in hands with low-grade fever and swelling of
lymph node

MOLLUSCUM CONTAGIOSUM

PREPARED BY: ROTHESSA CARINGAL, RMT 2

DNA VIRUSES

HERPES VIRUSES---------------------------------------------------------------------------
- “herpes” Gk. word : “to creep” (ulcerative lesions)
- latent infections or periodic reactivation, lifelong infections – HALLMARK
- reactivation could be activated by: stimuli, stress, caffeine and sunlight
- icosahedral (162 capsomeres), linear dsDNA, enveloped with peplomers (150-200 nm in size)
- diagnosed by presence of : cowdry type A intranuclear inclusion bodies (Lipschutz)

Four components:
1. Nucleic acid core
2. Capsid
3. Envelope
4. Tegument – asymmetric structure made of a
fibrous-like material which surrounds the capsid and
contains 20 different proteins

A. HERPES SIMPLEX VIRUS

a.1. HSV-1/HHV type 1
-TYPE 1: orofacialàtrigeminal dorsal root ganglia

a.2. HSV-2/HHV type 2

-TYPE 2: genitalàlumbosacral dorsal root ganglia

▪PATHOGENESIS
- mucoepithelial cells in skin and mucous membranes
- latent infection : innervating neurons
- vesicle formation
-skinàroot ganglia(reactivation depends on stimuli)
- reactivation: follows axons back to primary site
▪DIFFERENCES TYPE 1 vs TYPE 2
1.antigenic differences-
2.chick embryo CAM for type 2
3.chick embryo fibroblast cells
4.temperature sensitive ECZEMA HERPETICUM
5.more neurovirulent:
6.more resistant to antiviral agents
7.restriction endonuclease analysis of viral DNA
▪ CLINICAL FEATURES
1. Cutaneous infections
- napkin rash, fever blister, herpetic whitlow, herpes
gladiatorum, eczema herpeticum
2. Oral infection (HSV 1 & 2**) – presence of burning or
pain with vesicles, ulcers and crusted lesions
- acute gingivostomatitis, herpetic stomatitis,
pharyngitis, tonsillitis
HERPETIC WHITLOW
- ulcerations in buccal mucosa, posterior pharynx, gingival at
palatal mucosae
PREPARED BY: ROTHESSA CARINGAL, RMT 3
DNA VIRUSES

- Reactivation: lesions on the border of the lips and junction of oral mucosa and skin
3. Ophthalmic or ocular infections
- keratoconjuctivitis and corneal ulcers
4.Nervous system (olfactory bulb)
- HSV encephalitis, Sporadic encephalitis, HSV encephalitis, Guillain Barre syndrome
5. Visceral
- esophagitis, tracheobronchitis and pneumonitis, hepatitis, erythema multiforme
6. Genital infections (HSV 2)
- herpetic ulcers in genitals (male: glans/shaft/urethra WHILE female:vagina/cervix/perianal
area/inner thigh, FOR homosexuals: herpetic proctitis), urethra,
- carcinoma of the cervix
- Reactivation: infection at the same site
7. Neonatal herpes (transplacental infection) - mother to infant transmission through vaginal delivery
- Cesarean delivery will reduce risk of transmission
8. Immunocompromised hosts
▪ LAB DIAGNOSIS
1. Specimens – punctured herpes lesion/vesicle absorbed in swab, brain biopsy
- Placed in viral transport media OR refrigerated/frozen at -70C
2. Microscopy
a. Tzanck smear

-rapid, fairly sensitive, inexpensive

- smears should be from base of vesicles
-stain: 1% aqueous sol’n of toluidine blue for
15 secs
- (+)cytopathologic effects: “ballooning of
cytoplasm”
- (+)Cowdry type A intranuclear inclusions
-(+) multinucleated giant cells with faceted
nuclei and homogenously stained ‘ground
glass’ chromatin (Tzanck cells)
b. EM
c. Fluorescent antibody technique: brain biopsy
3. Virus Isolation
- human diploid fibroblasts (24-48 hrs but observation for two weeks)
4. Direct antigen testing – rapid, sensitive, inexpensive
- HSV antigen mixed with HSV-specific antibody detected using ID or IP
5. PCR – detection of viral DNA; More sensitive than cell culture and DAT
6. Intracerebral inoculation (rabbits & mice)
7. corneal scarification à
8. tissue cultureà
à
9. chick embryo CAMà
10. Gold standard: cell cultures: A-549, HEp-2 or MRC-5 cell lines
- Depends on the quality of sample and manner of collection
- Samples are to be inoculated within 1 hour after collection
- Growth: round, refractile CPE within 1-2 days of inoculation
11. ELVIS (enzyme-linked, virus-inducible system) test - a gene for the enzyme β-galactosidase linked
to a virus-induced promoter has been inserted into baby hamster kidney cells

PREPARED BY: ROTHESSA CARINGAL, RMT 4

DNA VIRUSES

▪ TREATMENT
- Idoxuridine (eye and skin infections)
- acyclovir and vidarabine(deep&systemic infections)
- valaciclovir and famciclovir (oral infections)

B. HERPES VIRUS SIMIAE: B VIRUS

- Herpes B for Old World monkeys
- Sabin and Wright discovered this from a brain
- fatal ascending myelitis

C. VARICELLA ZOSTER VIRUS (HHV TYPE 3) – the “CLASSIC” childhood disease

- chickenpox, herpes zoster/shingles
- chickenpox vs zoster (they are morphologically identical)
c.1. Varicella (Chickenpox)
- mildest, highly communicable, most common childhood infection
- infects conjunctiva or mucosa of the upper respiratory tract and then travels to the lymph nodes
- INCUBATION PERIOD (4-6 days after initial infection): infected T cells enter bloodstream
causing PRIMARY VIREMIA and infect organs
- SECONDARY VIREMIA (14 days after initial infection): infects skin cells causing vesicular
rash
- S/S: fever and malaise before the appearance of maculopapular rash
- rash appears mainly in HEAD and TRUNK and very
superficial
- crusting of rash appears 48 hrs for its maturity
- the virus affects SENSORY GANGLIA for its latency
(“hides” in CNS)
- primary infection is severe in adults: hemorrhagic rash
- varicella pneumonia in adults and different
complications: myocarditis, acute cerebellar ataxia,
meningitis and encephalitis, secondary bacterial infections,
Reyes’ syndrome
c.2. Herpes zoster (shingles/zona) – RECURRENCE OF VZV HEMORRHAGIC RASH
- disease of old age (>45yo)
- occurs in persons who had chickenpox
- latency in sensory ganglia that follows an anatomic route along torso infecting neurons to skin
- starts with severe pain in the area of the skin or mucosa supplied by the sensory nerves and
ganglia (common with D3 to L2 to trigeminal nerve segments)
- accompanied by a POSTHERPETIC NEURALGIA – a chronic, debilitating pain caused by
VZV destruction of neurons
▪ COMPLICATIONS
1. postherpetic pain
2. ophthalmic zoster
3. generalized zoster
4. Ramsay Hunt syndrome – affects facial nerve and erupts in the tympanic membrane, external auditory
canal and often a facial palsy

▪ LAB DIAGNOSIS (usually clinical) – Specimen collected by scraping the base of a fresh vesicular lesion
1. Microscopy- demonstration of multinucleated giant cells and Cowdry tpe A intranuclear inclusion
bodies (Tzanck, Giemsa, HE stain)

PREPARED BY: ROTHESSA CARINGAL, RMT 5

DNA VIRUSES

2. Cell culture (MRC-5, HF and A549 cell lines) – CPE of small clusters of ovoid cells in fibroid cells
- SIMPLIFIED METHOD: Shell vial cultures
-cover slips with MRC-5 cells attached in a monolayer incubated for 3-6 days; coverslip
is fixed with acetone and is stained with fluorescein isothiocyanate-conjugated (FITC)
monoclonal IgG specific antibody
- positive: cytoplasmic, apple green fluorescence in fluorescent microscope
3. Virus antigen (IF, CIE, ELISA, **multiplex PCR)
4. Serological diagnosis (rise in the ab titer)
▪ PROPHYLAXIS AND TREATMENT
1. Active immunization -live attenuated varicella vaccine administered through subcutaneous injection
2. Passive immunization - VZIG

C. EPSTEIN BARR VIRUS (HHV TYPE 4) - MOST “SINISTER” HERPESVIRUS

- discovered during a search for the cause of Burkitt’s
lymphoma
- associated with malignant disease :
- EBV infected B cells capable to grow in vitro
- B cells with cell death and release of mature progeny
virions
- classic lymphocytosis: activation and proliferation of T
cells à atypical T cells/ reactive lymphocytes
(Downey cells)
- MOST SIGNIFICANT CLINICAL EFFECT: B-cell lymphoproliferative disorder or LYMPHOMA
▪ CLINICAL CONDITIONS
1.Infectious Mononucleosis (Glandular Fever)
- aka KISSING DISEASE
- high fever, sore throat, headache, malaise, fatigue, lymphadenopathy and splenomegaly
- maculopapular rash with ampicillin
- happens with adolescents and young adults when sharing saliva, often by kissing
- complications may occur as airway obstruction, splenic rupture, neurological complications
- IgM à IgG à IgA antibody proliferation
2.Oral Hairy Leukoplakia -wartlike lesions in tongue in HIV infected persons
3. Chronic Disease - cyclic recurrent disease in some people
4. Burkitt’s lymphoma - tumor of jaw in African children and young adults
- EBV DNA and EBNA1 antigen; elevated Anti-EA/R IgG antibody
- cofactor:_________
5. Nasopharyngeal carcinoma (NPC) **- Chinese males in origin; EBNA
6. Lymphoproliferative Diseases in Immunodeficient Host - fatal: AIDS
▪ LAB DIAGNOSIS
1. Differential White Cell Count - leukoPENIA in INITIAL phase
- leukoCYTOSIS with atypical mononuclear cells in LATER INFECTION
2. Paul Bunnell Test – detection of nonspecific heterophile antibodies Burkitt’s lymphoma

PREPARED BY: ROTHESSA CARINGAL, RMT 6

DNA VIRUSES

3. EBV Specific Antibodies –

a. anti-VCA (antibodies against viral capsid antigen) – IgM / IgG
b. Anti-EA IgG (IgG antibody to early antigen) – acute phase/current/recent
c. Anti-EA/D (antibody to early antigen; diffuse) – acute phase; **NPC have elevated IgG and
IgA anti-EA/D antibodies
d. Anti-EA/R (antibody to early antigen, restricted) – acute phase but disappear soon after
anti-EA/D; can persist for years
e. Anti-EBNA (antibody to the EBV nuclear antigen) – antibodies appear about 1 month after
infection

Paul Bunnell Anti-VCA IgM Anti-VCA IgG Anti-EA IgG Anti-EBNA Interpretation
- - - - - No exposure
+ + + +/- - Acute IM
+/- +/- + +/- + Recent infection
- - + - + Past infection

4. Antigen Detection – EBV antigen

5. PCR – QUALI & QUANTI - Nucleic acid extracted from patient specimens is amplified and detected
by polymerase chain reaction (PCR) and fluorescent resonance energy transfer (FRET) probe
detection.

D. CYTOMEGALOVIRUS (HHV type 5) – common cause of CONGENITAL BIRTH DEFECTS

- salivary gland viruses
- transmission: congenital, oral, sexual, blood transfusion, tissue transplant
- normal hosts: older children and adults
- immunocompromised hosts: IM-like illness
- congenital and perinatal infections: intrauterine infectionà fatal death or cytomegalic inclusion: CNS
& RES involvement
- intrauterine growth retardation, deafness, intellectual impairment, jaundice, hepatosplenomegaly,
thrombocytopenia, cerebral calcification, microcephaly
- perinatal infection:acquired from genital secretions or breast milk
- postnatal infection: saliva, sexual, blood transfusion and donated organs
▪ LAB DIAGNOSIS
1. Specimens: urine, saliva, breast milk, semen, cervical secretion and buffy coat
2. TORCH panel – disease screening of infants
3. Demonstration of cytomegalic cell: hallmark
- owl’s eye basophilic intranuclear inclusion body stained using PAPs and HE stain
4. Isolation of virus - human fibroblast cell cultures (1-2 weeks incubation)
- (+) CPE: swollen refractile cells with cytoplasmic granules
- “CENTRIFUGATION-AMPLIFIED SHELL VIALS” : modification, diagnosis w/in 24-48hrs
5. DNA probes: CMV antigens
- detection of 65-kDa lower matrix phosphoprotein (pp65)
in the nuclei of infected peripheral WBCs
6. PCR: genome detection
7. Serology: ELISA detection of IgM abs
▪ TREATMENT: ganciclovir and foscarnet, PROPER screening of blood
and organ donors AND administration of CMV Igs
Fluoresceing WBC containing CMV
antigens in CMV antigenemia stain (DNA
probing

PREPARED BY: ROTHESSA CARINGAL, RMT 7

DNA VIRUSES

E. HHV type 6
- first isolated in pxs with AIDS
-lymphotropic and ubiquitous
-saliva and spread by oral secretions
- two variants: A and B
- variant B: cause of EXANTHEMA SUBITUM OR ROSEOLA INFANTUM OR SIXTH DISEASE
- isolated from peripheral blood mononuclear cells in early febrile stage with maculopapular rash
- IF using monoclonal antibodies for viral ag detection

F. HHV type 7 - ORPHAN VIRUS

-transmitted thru saliva; infects CD4 receptor on T cells
-resembles IM/exanthema subitum

G. HHV type 8 – HIV-associated Kaposi sarcoma

- aka Kaposi’s sarcoma associated herpesvirus (KSHV)
- vascular tumors of mixed cellular composition (appearance of
erythematous or purplish nodules and indurated plaques)
that can spread in lungs, GI tract and other organs
-involved in body cavity-based lymphomas in AIDS px
- sexual interaction (men to men)
- PCR: viral DNA

HERPES VIRUS DISEASE TRANSMISSION LATENCY

HSV 1 & 2 Orofacial and Direct contact Sensory nerve
genital herpes ganglia
Varicella Zoster Chickenpox / Close personal Dorsal root ganglia
Virus Shingles contact, respiratory
Epstein Barr Virus Infectious Close contact with B lymphocytes
mononucleosis infected saliva
Cytomegalovirus Congenital disease Close contact with WBCs, Endothelial
of the newborn, infected secretions, cells, Cells of
Heterophile-NEG Blood transfusion, different organs
IM (WBCs), Organ
transplant,
transplacental
Herpes virus 6 and Roseola (Exanthem Close contact via CD4 cells / T
7 (HHV-6 and subitem/Sixth respiratory route lymphocytes
HHV-7) disease)
Human herpesvirus Kaposi’s sarcoma Not known Viral genome found
8 (HHV-8) in Kaposi’s tumor
cells, endothelial
cells, and tumor-
infiltrating
leukocytes

PARVOVIRUSES-----------------------------------------------------------------------------
-smallest DNA virus, nonenveloped/naked, icosahedral, ssDNA but appear spherical in EM
-two subfamilies: Parvovirinae and Densovirinae
-three genera of Parvovirinae: (1) Parvovirus, (2)Dependovirus and (3) Erythrovirus
A. PARVOVIRUS
- autonomous replication : FPV and CPV – imp’t in vetmed
PREPARED BY: ROTHESSA CARINGAL, RMT 8
DNA VIRUSES

B. DEPENDOVIRUS
-requires helper virus for replication, aka AAV
C. ERYTHROVIRUS (parvovirus B19) – the only human pathogen among Parvoviridae
- cell receptor:_____ (named after its serum sample:_____________________________________ )
- replication present in RBC, erythroid precursors, vascular endothelium, adult BM and fetal liver cells
-transmission: respiratory route THUS highly contagious
D. Human Bocavirus (HBoV) – novel parvorvirus discovered in 2005 causing URTI and LRTI
- present coinfection with RSV
- S/S: cough, rhinorrhea, fever, difficulty breathing, diarrhea, conjunctivitis, and rash
■ CLINICAL DISEASES
1. Minor illness: NS respiratory tract illness

2. Erythema infectiosum (Fifth disease) – B19 infection

- erythematous maculopapular rash (slapped cheek appearance in face)
- infects two type of cells:
(1)
(2)
3. Joint disease
4. Aplastic crisis with chronic hemolytic anemia – decreased production (risk for blood donors)
5. Infection during pregnancy
6. Infections in immunosuppressed
■ PATHOGENESIS – Biphasic illness
First phase: marked fever, malaise, myalgia and chills – signal for peak levels of virus and destruction of RBC
Second phase: rash and arthralgia – virus disappeared but oparvovirus-specific antibody is present
- Rash appears because of the immune complex deposition in capillaries
■ LAB DIAGNOSIS
1.Virus isolation
2. Detection of viral NA
3. Antigen detection
4. Antibody detection

ADENOVIRUSES-----------------------------------------------------------------------------
-medium sized (70-90nm), NE, linear dsDNA, icosahedral
-“adenoid”
-apical fibers: space vehicle
-viably stable at 37’C for a week; inactivated at 50’C
- Mastadenovirus : 52 serotypes: A to G serotypes
■ CLINICAL MANIFESTATIONS
A. Respiratory Diseases
- Pharyngitis, Pneumonia, Colds, Tonsillitis,
Acute Respiratory Diseases - Croup
B. Eye infections
- Pharyngoconjunctival fever, Epidemic
keratoconjunctivitis, Acute follicular conjunctivitis with ear infections
C. Other Diseases
1. Mesenteric adenitis
2. Intussusception
3. Pertussis-like illness
4. Acute hemorrhagic cystitis
5. Gastroenteritis – serotypes 40 & 41 (they are called “Enteric adenoviruses”)
D. Systemic Infection in Immunocompromised Patients Include Pneumonia and Hepatitis

PREPARED BY: ROTHESSA CARINGAL, RMT 9

DNA VIRUSES

■ TRANSMISSION: Aerosolized droplet or airborne

■ LAB DIAGNOSIS
1. Specimens: eye secretions, respiratory tract, stool and urine
2. Direct Demonstration of Virus
*EM
*Viral ag
*Viral DNA
*Latex agglutination
3. Cell cultures – A-549, Hep-2 and He-La cells – producing grapelike cluster CPE
4. PCR
5. Serology – IFA, EIA
■ TREATMENT: live oral vaccines for military (serotypes 4 and 7)

PAPOVAVIRUSES---------------------------------------------------------------------------
-Pa -Po -Va
-two genera: Papillomavirus and Polyomavirus

A. PAPILLOMAVIRUSES – common cause of sexually transmitted diseases

- small, nonenveloped, circular, dsDNA
- larger than polyomaviruses
-induce hyperplastic epithelial lesions
- 200 genotypes but 80 are well-characterizes types of HPV
-causes different kinds of human warts (exhibition of tissue tropism for either cutaneous or mucosal)
1. Cutaneous warts
-plantar warts (HPV-1)
-flat warts
-common warts (HPV-2 & 4)
*Epidermodysplasia verruciformis
2. Anogenital warts (HPV-6 and HPV-11)
-aka:_______________________
-women: vulva, vagina, cervix
-men: shaft, penis, perianal skin and anal canal
-benign vulval or penile warts:
-cervical and anogenital warts
3. Recurrent Respiratory Papillomatosis
- benign squamous papillomata
- infected birth canal for children
- orogenital contact for adults

4. Oral Papillomatosis
-oral florid papillomatosis
5. Cancer

-HPV DNA
-low-grade cancer:
-greater severity and invasive cancer
- HPV types 16 & 18
■ TRANSMISSION: sexually transmitted or direct contact
■ LATENCY: epithelial tissue
■ LAB DIAGNOSIS
1. Morphological ID Papilloma viruses cannot be grown in cell cultures.
Cytologic examinations would look for koilocytes,
1.1 Cytological and histological detection cells with perinuclear clearing accompanied by an
PREPARED BY: ROTHESSA CARINGAL, RMT increased density of the surrounding rim of 10
cytoplasm, which are indicative of HPV infection
DNA VIRUSES

1.2. Immunocytochemical detection

1.3.Molecular methods such as DNA probe
- HPV DNA Koilocytes
2. Serology
■ TREATMENT: vaccines: Cervarix and Gardasil – derivative of the protein viral coat and immunity to HPV16

B. POLYOMAVIRUSES
- smaller, circular dsDNA, NE, icosahedral
-poly: oma:
- capable for latency however can be reactivated by immunosuppression
1. Mouse Polyomavirus
2. Simian vacuolating virus -isolated from uninoculated rhesus and cynomolgus monkey tissue cultures
- exposure was a result of administration of SV40-contaminated Salk polio vaccine
3. JC virus – infect humans
-brain of patient with Hodgkin’s disease and PML
- named to the patient to whom it was isolated: __________________________________
- cause of Progressive Multifocal Leukoencephalopathy (PML)
- latency: B LYMPHOCYTES
- REACTIVATION: CNS disease
4. BK virus – infect humans
- isolated from immunocompromised patient
- named after the person whom it was isolated
- isolated from urine of patient with kidney transplant
- latency: KIDNEY
- REACTIVATION: hemorrhagic cystitis
5. OTHER NEWLY DISCOVERED: KI virus, MC virus and WU virus
- identified through molecular methods in specimens – respiratory secretions and stool
- pathogenicity and prevalence still not known
* MC virus – causes Merkel cell carcinoma (respiratory specimens)
■ LAB DIAGNOSIS
1. EM
JC virus-
BK virus-
2. Virus Isolation
JC virus-
BK virus-
3. Viral ag detection
4. Viral NA detection (PCR)
JC virus-
BK virus-
5. Cytopathology

REFERENCES:
- Essentials of Diagnostic Microbiology
- Bailey and Scott’s
- Textbook of Diagnostic Microbiology by Mahon, Lehman and Manuselis (5th Ed)

PREPARED BY: ROTHESSA CARINGAL, RMT 11