No Enveloped DNA Viruses: Papillomaviruses and Polyomaviruses
No Enveloped DNA
Viruses
Dr. Luma Amer
Papillomaviruses
Human papillomavirus (HPV) causes papillomas, which are benign tumors of squamous
cells (e.g., warts on the skin). Some HPV types, especially types 16 and 18, cause carcinoma
of the cervix, penis, and anus.
Common seed warts
– painless, elevated, rough
growth; on fingers, etc.
Plantar warts – deep
, painful; on soles of feet
Genital warts -morphology
ranges from tiny, flat,
like masses .
No enveloped DNA Viruses
Adenoviruses
Papillomaviruses
Polyomaviruses
Parvoviruses
Polyoimaviruses
Induce tumors in experimental animals
JC(john Cunningham) Common infection of childhood; persists in kidney epithelium, lymphocytes, and
bone marrow; produces PML(progressive multifocal leukoencephalopathy) in immuno-compromised hosts
BK viruses most important human polyomas, Common infection of childhood; persists in kidney
epithelium and possibly lymphocytes BK infection in renal transplants causes complications in urinary
function
Common throughout the world
Majority of infections are asymptomatic or mild
Progressive multifocal leukoencephalopathy (PML) is an uncommon fatal infection by JC
Important Properties
Papillomaviruses :
Nonenveloped viruses .
Double-stranded circular DNA .
An icosahedral nucleocapsid .
The HPV genome has seven early genes (E1–E7) and two late
genes (L1 and L2). The early genes encode proteins involved in
the synthesis of viral mRNA and in the replication of the
progeny DNA genomes, and the late genes encode the structural
proteins of the progeny virions
Two of the early genes,
E6 and E7
, are implicated in carcinogenesis.
They encode proteins that
inactivate
proteins encoded by tumor
suppressor genes
in human cells (e.g., the p53 gene and the
retinoblastoma [RB] gene, respectively).
Inactivation of the p53 and
RB proteins is an important step in the process by which a normal cell
becomes a cancer cell.
There are at least 100 types of papillomaviruses, classified primarily
on the basis of DNA restriction fragment analysis .For example, skin
warts are caused primarily by HPV-1 through HPV-4, whereas genital
warts are usually caused by HPV-6 and HPV-11. Approximately 30
types of HPV infect the genital tract.
Summary of Replicative Cycle
After attachment and uncoating, the genome DNA moves to the nucleus.
Messenger RNA is synthesized by host cell RNA polymerase with early viral protein
E2 acting as a transcriptional activator.
Early viral protein E1 acts as a
helicase
that separates the DNA strands of the incoming
viral genome.
This allows the host cell
DNA polymerase
to synthesize the progeny DNA genomes.
The 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.
In human tissues, infectious virus particles are found in the
terminally differentiated squamous cells rather than in the basal
cells .
Note that HPV initially infects the cells of the basal layer in the
skin, but no virus is produced by the basal cells.
Papilloma virus and malignant:
In malignant cells :
Viral DNA is integrated into host cell DNA in the vicinity of
cellular proto-oncogenes.
E6 and E7 are overexpressed .
However, in latently infected, nonmalignant cells, the viral
DNA is episomal, and E6 and E7 are not overexpressed
. This
difference occurs because another early gene, E2, controls E6
and E7 expression.
The E2 gene is functional when the viral DNA is episomal but
is inactivated when it is integrated
.
Transmission & Epidemiology:
Papillomaviruses are transmitted primarily by skin-to-skin contact, including
genital contact.
HPV transmitted from an infected mother to the neonate during childbirth
causes warts in the mouth and in the respiratory tract, especially on the
larynx, of the infant.
Many species of animals are infected with their own types of
papillomaviruses, but these viruses are not an important source of human
infection.
Pathogenesis & Immunity
Most warts are benign and do not progress to malignancy.
HPV infection is associated with carcinoma of the uterine cervix and penis.
The proteins encoded by viral genes E6 and E7 interfere with the
growth-inhibitory activity of the proteins encoded by the p53 and RB
tumor suppressor genes and thereby contribute to oncogenesis by these
viruses.
The E6 and E7 proteins of HPV-16 bind more strongly to p53 and RB
proteins than the E6 and E7 proteins of HPV types not implicated in
carcinomas—a finding that explains why HPV-16 causes carcinomas more
frequently than the other types of HPV.
Laboratory Diagnosis :
Infections are usually diagnosed clinically. The presence of koilocytes in the
lesions indicates HPV infection.
PCR-based test can be used to detect the presence of the DNA of 14 high-
risk genotypes, including HPV-16 and HPV-18.
Diagnostic tests based on detection of antibodies in a patient’s serum or on
isolation of the virus from a patient’s tissue are not used.
Explore the characteristics and implications of no enveloped DNA viruses, such as Papillomaviruses causing common warts and Polyomaviruses inducing tumors in animals. Learn about their genetic properties, potential for carcinogenesis, and infections in different host systems.
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Presentation Transcript
No Enveloped DNA Viruses Dr. Luma Amer
Papillomaviruses Common seed warts painless, elevated, rough growth; on fingers, etc. Plantar warts deep, painful; on soles of feet Genital warts -morphology ranges from tiny, flat, like masses .
No enveloped DNA Viruses Adenoviruses Papillomaviruses Polyomaviruses Parvoviruses
Polyoimaviruses Induce tumors in experimental animals JC(john Cunningham) Common infection of childhood; persists in kidney epithelium, lymphocytes, and bone marrow; produces PML(progressive multifocal leukoencephalopathy) in immuno-compromised hosts BK viruses most important human polyomas, Common infection of childhood; persists in kidney epithelium and possibly lymphocytes BK infection in renal transplants causes complications in urinary function Common throughout the world Majority of infections are asymptomatic or mild Progressive multifocal leukoencephalopathy (PML) is an uncommon fatal infection by JC
Important Properties Papillomaviruses : Nonenveloped viruses . Double-stranded circular DNA . An icosahedral nucleocapsid . The HPV genome has seven early genes (E1 E7) and two late genes (L1 and L2). The early genes encode proteins involved in the synthesis of viral mRNA and in the replication of the progeny DNA genomes, and the late genes encode the structural proteins of the progeny virions
Two of the early genes, E6 and E7, are implicated in carcinogenesis. They encode proteins that inactivate proteins encoded by tumor suppressor genes in human cells (e.g., the p53 gene and the retinoblastoma [RB] gene, respectively). Inactivation of the p53 and RB proteins is an important step in the process by which a normal cell becomes a cancer cell. There are at least 100 types of papillomaviruses, classified primarily on the basis of DNA restriction fragment analysis .For example, skin warts are caused primarily by HPV-1 through HPV-4, whereas genital warts are usually caused by HPV-6 and HPV-11. Approximately 30 types of HPV infect the genital tract.
Summary of Replicative Cycle After attachment and uncoating, the genome DNA moves to the nucleus. Messenger RNA is synthesized by host cell RNA polymerase with early viral protein E2 acting as a transcriptional activator. Early viral protein E1 acts as a helicase that separates the DNA strands of the incoming viral genome. This allows the host cell DNA polymerase to synthesize the progeny DNA genomes. The 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.
In human tissues, infectious virus particles are found in the terminally differentiated squamous cells rather than in the basal cells . Note that HPV initially infects the cells of the basal layer in the skin, but no virus is produced by the basal cells.
Papilloma virus and malignant: In malignant cells : Viral DNA is integrated into host cell DNA in the vicinity of cellular proto-oncogenes. E6 and E7 are overexpressed . However, in latently infected, nonmalignant cells, the viral DNA is episomal, and E6 and E7 are not overexpressed. This difference occurs because another early gene, E2, controls E6 and E7 expression. The E2 gene is functional when the viral DNA is episomal but is inactivated when it is integrated.
Transmission & Epidemiology: Papillomaviruses are transmitted primarily by skin-to-skin contact, including genital contact. HPV transmitted from an infected mother to the neonate during childbirth causes warts in the mouth and in the respiratory tract, especially on the larynx, of the infant. Many species of animals are infected with their own types of papillomaviruses, but these viruses are not an important source of human infection.
Pathogenesis & Immunity Most warts are benign and do not progress to malignancy. HPV infection is associated with carcinoma of the uterine cervix and penis. The proteins encoded by viral genes E6 and E7 interfere with the growth-inhibitory activity of the proteins encoded by the p53 and RB tumor suppressor genes and thereby contribute to oncogenesis by these viruses. The E6 and E7 proteins of HPV-16 bind more strongly to p53 and RB proteins than the E6 and E7 proteins of HPV types not implicated in carcinomas a finding that explains why HPV-16 causes carcinomas more frequently than the other types of HPV.
Laboratory Diagnosis : Infections are usually diagnosed clinically. The presence of koilocytes in the lesions indicates HPV infection. PCR-based test can be used to detect the presence of the DNA of 14 high- risk genotypes, including HPV-16 and HPV-18. Diagnostic tests based on detection of antibodies in a patient s serum or on isolation of the virus from a patient s tissue are not used.
