PAPOVAVIRUS FAMILY
(PAPOVAVIRIDAE) :
NOW 2 FAMILIES
Papillomaviruses and
Polyomaviruses
HUMAN PAPILLOMAVIRUSES (HPVS):
Warts
human
cancer (e.g.,
cervical carcinoma):
 several genotypes
POLYOMAVIRIDAE
 BK
and JC viruses,
usually asymptomatic infection
 in



immunosuppressed people :
BK: renal disease
JC: progressive multifocal
leukoencephalopathy (PML),
Simian virus 40 (SV40)
UNIQUE PROPERTIES OF
POLYOMAVIRUSES AND
PAPILLOMAVIRUSES
 Small
 Double-stranded
genome
circular DNA
UNIQUE PROPERTIES OF POLYOMAVIRUSES AND
PAPILLOMAVIRUSES
 Viruses
encode proteins that promote
cell growth
 These proteins bind to the cellular
growth-suppressor proteins p53 and
p105RB (p105 retinoblastoma gene
product).


Papilloma E6 binds to p53, and
Papilloma E7 binds to p105RB
UNIQUE PROPERTIES OF POLYOMAVIRUSES AND
PAPILLOMAVIRUSES
 lytic
infections
 Persistent
 latent infections
 immortalize (transform) cells
HUMAN PAPILLOMAVIRUSES (HPV)
 More
than 100 genotypes
 HPV can be distinguished further as
cutaneous HPV or mucosal HPV on the
basis of the susceptible tissue. Within the
mucosal HPV, there is a group associated
with cervical cancer.
HPV
 infect
and replicate in the squamous
epithelium of skin (warts) and
 mucous membranes (genital, oral,
and conjunctival papillomas) to
induce epithelial proliferation.
TRANSMISSION
HPV
resists inactivation
can be transmitted on fomites,
such as the surfaces of
countertops or furniture,
bathroom floors, and towels
Asymptomatic shedding may
promote transmission.
TRANSMISSION
HPV
(1)
(2)
(3)
infection is acquired
by direct contact through
small breaks in the skin or
mucosa
during sexual intercourse
while an infant is passing
through an infected birth
canal.
DISEASE MECHANISMS OF PAPILLOMAVIRUSES
AND POLYOMAVIRUSES
PAPILLOMAVIRUSES
 Virus
is acquired by close contact and
infects the epithelial cells of the skin or
mucous membranes.
 Tissue tropism and disease presentation
depend on the papillomavirus type.
 Virus persists in the basal layer and then
produces virus in terminally
differentiated keratinocytes.
 Viruses cause benign outgrowth of cells
into warts.
DISEASE MECHANISMS OF PAPILLOMAVIRUSES
AND POLYOMAVIRUSES
PAPILLOMAVIRUSES
 HPV
infection is hidden from immune
responses and persists.
 Warts resolve spontaneously, possibly as a
result of immune response.
 Certain types are associated with
dysplasia that may become cancerous
with the action of cofactors.
 DNA of specific HPV types is present
(integrated) in the tumor cell
chromosomes.
POLYOMAVIRUSES (JC AND BK VIRUSES)
 Virus
is probably acquired through
the respiratory route and spread by
viremia to the kidneys early in life.
 Infections
 Virus
are asymptomatic.
establishes persistent and
latent infection in organs such as
the kidneys and lungs.
POLYOMAVIRUSES (JC AND BK VIRUSES)
 In
immunocompromised people,

BK: Renal infection(hematuri)

JC virus is activated, spreads to the
brain, and causes progressive
multifocal leukoencephalopathy
(PML), a conventional slow virus
disease.
EPIDEMIOLOGY OF POLYOMAVIRUSES AND
PAPILLOMAVIRUSES
 Disease/Viral
Factors
 Capsid virus is resistant to inactivation
 Virus persists in host
 Asymptomatic shedding is likely
 Transmission
 Papillomavirus: direct contact, sexual
contact (sexually transmitted disease) for
certain virus types, or passage through
infected birth canal for laryngeal
papillomas (types 6 and 11)
 Polyomavirus: inhalation or contact with
contaminated water
EPIDEMIOLOGY OF POLYOMAVIRUSES AND
PAPILLOMAVIRUSES
 Who
Is at Risk?
 Papillomavirus: warts are common;
sexually active people are at risk for
infection with HPV types correlated
with oral and genital cancers
 Polyomavirus: ubiquitous;
immunocompromised people
HUMAN PAPILLOMAVIRUS
is possibly the most prevalent sexually
transmitted infection in the world,
 with certain HPV types common among sexually
active people.
 At least 20 million people in the United States
are infected with HPV, with approximately 6
million new genital cases per year.

HPV
HPV
is present in 99.7% of all
cervical cancers.
HPV-16, HPV-18, HPV-31, and
HPV-45 are high-risk
the second leading cause of
cancer death in women
HPV
 10%
of women infected with the
high-risk HPV types will develop
cervical dysplasia, a precancerous
state.
Major risk factors for infection and
progression to cancer:
 Multiple sexual partners
 smoking
 a family history of cervical cancer
 immunosuppression
HPV DISEASES
 Cutaneous
 Skin
Syndromes
warts
 Mucosal Syndromes
 Benign head and neck tumors
 Laryngeal papilloma
 Oral papilloma
 Conjunctival papilloma
 Anogenital warts
 Condyloma acuminatum 6, 11
 Cervical intraepithelial neoplasia,
cancer16, 18
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© 2005 Elsevier
Downloaded from: StudentConsult (on 11 May 2009 01:13 PM)
© 2005 Elsevier
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© 2005 Elsevier
Downloaded from: StudentConsult (on 11 May 2009 01:13 PM)
© 2005 Elsevier
LABORATORY DIAGNOSIS OF
PAPILLOMAVIRUS INFECTIONS

Cytology:PAP smear:Koilocytotic cells

Polymerase chain reaction Viral nucleic acid
KOILOCYTES
characteristic of papillomavirus infection,
 are enlarged keratinocytes with clear haloes
around shrunken nuclei

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© 2005 Elsevier
VACCINE:
Vaccine:
http://www.cdc.gov/hpv/
 tetravalent HPV vaccine
(Gardasil) :HPV 6, 11, 16, and
18 can prevent infection and
hence reduce the incidence of
anogenital warts and cervical
cancer.
 Bivalent HPV(Cervarix)(16,18)
 A series of three immunizations is
recommended for girls ( boys), starting
at age 11 prior to sexual activity.
VACCINE
 The
HPV vaccine is not a
replacement for a PAP smear,
and women should continue to be
tested.
 At present, the best way to prevent
transmission of warts is to avoid
coming in direct contact with
infected tissue. Proper precautions
(e.g., the use of condoms) can
prevent the sexual transmission of
HPV!!!!