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Virology Quiz 4 > Tumor Viruses > Flashcards

Tumor Viruses Flashcards

1
Q

Oncogenic Viruses

A

A number of different viruses are capable of causing
cancer in animals. Cancer-causing viruses are called oncogenic viruses, and historically have been classified into two groups based on the type of nucleic acid genome they have.

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2
Q

Types of Oncogenic Viruses

A
  • RNA tumor viruses have an RNA genome and belong to two families – retroviruses or flaviviruses.
  • DNA tumor viruses belong to several different families and have the common feature of a DNA genome.
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3
Q

Viruses and the cancer they cause

Retrovirus

A

• Genome: RNA
• Member: Human T-cell leukemia virus-1,2
• Cancer: Cutaneous T-cell lymphoma; Adult T-cell
leukemia

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4
Q

Viruses and the cancer they cause

Flatvirus

A
  • Genome: RNA
  • Member: Hepatitis C virus
  • Cancer: Hepatocellular carcinoma
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5
Q

Viruses and the cancer they cause

Papovavirus

A
  • Genome: DNA
  • Member: Human Papilloma Virus
  • Cancer: Cervical Carcinoma
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6
Q

Viruses and the cancer they cause

Herpesvirus

A

• Genome: DNA
• Member: Epstein Barr virus; Kaposi’s sarcoma herpesvirus
• Cancer: -Burkitt’s Lymphoma; Nasopharyngeal
carcinoma; Kaposi’s sarcoma

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7
Q

Viruses and the cancer they cause

Hepadnavirus

A
  • Genome: DNA
  • Member: Hepatitis B Virus
  • Cancer: Hepatocellular carcinoma
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8
Q

General Properties of Tumor Viruses

A

• Tumor viruses cause cancer in laboratory
animals, and also cause cells grown in tissue culture to undergo transformation.
• In most (but NOT all) cases, a viral gene, called an oncogene, is responsible. Frequently, the viral oncogene is integrated into the host cell chromosomal DNA.
• Expression of the viral oncogene product disrupts
regulation of cellular growth control.

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9
Q

Transformation (In Vitro)

A
  • Immortal: can grow indefinitely
  • Reduced requirement or serum
  • Loss of ability to be growth arreseted
  • Grow to high densities
  • Loss of contact inhibition
  • Anchorage independent (soft agar assay)
  • Altered morphology
  • Tumorigenic
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10
Q

Detection of Oncogenic Viruses in Tumors

Infectious Virus

A

Infectious virus may be detected by preparing a cell free extract of a tumor, and:
a. Testing for its ability to cause tumors when injected into laboratory animals.
b. Determining its ability to cause transformation
of tissue culture cells.

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11
Q

Detection of Oncogenic Viruses in Tumors

Viral Proteins

A

Viral proteins may be detected by immunological
methods, e.g. fluorescent antibodies, western
blotting, ELISA.

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12
Q

Detection of Oncogenic Viruses in Tumors

Viral Nucleic Acid

A

Viral nucleic acid may be detected by northern

blotting, Southern blotting, or PCR.

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13
Q

Differences between normal cells and Cancer cells

A

• Morphology – Normal cells grow in an orderly
way, are often flat in culture. Cancer cells are
rounded, and grow in a disordered way.
• Biochemistry – Cancer cells have an increased
rate of glycolysis and glucose transport. Cancer cells often have loss of actin filaments, secrete high levels of proteinases and have reduced surface fibronectin.
• Growth – Cancer cells do not exhibit contact
inhibition, and continue to divide after they touch each other. Also cancer cells have a reduced
requirement for extracellular growth factors or serum.

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14
Q

DNA Tumor Viruses

A

• Many viruses grow better in cell that are actively
synthesizing DNA. However most cells in the
body are quiescent and not dividing.
• Several DNA viruses encode genes that
‘push’ the host cell into the cell cycle by modifying
host proteins or gene expression.
• Normally this results in death of the cell and
production of more virus, however rarely this can result in transformation of host cells.
• They interfere with tumor supressors by commonly targeting p53 and Rb

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15
Q

Papoviruses

A

The papovaviruses are small, naked, icosahedral
viruses with a double-stranded, circular DNA genome [< 10 kilobases]. The small papovavirus genome encodes fewer than 10 genes, and thus this family relies greatly on host proteins (such as DNA polymerase and RNA polymerase) for replication and gene expression.
All papovavirus genes are essential for virus
growth.

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16
Q

Examples of Papoviruses

A
  • Papilloma virus (humans, many other mammals)
  • Polyoma virus (rodents)
  • SV40 (monkeys)
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17
Q

Classes if genes in Papoviruses

A

Papovaviruses have two classes of genes:
• early genes
• late genes.

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18
Q

Early Genes in Papoviruses

A

With SV40, the large T-antigen gene is expressed
early. T-antigen recognizes the start site for SV40 DNA replication (origin of replication) and binds to it. Host DNA-directed DNA polymerase then binds to T-antigen and starts viral DNA replication.

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19
Q

Late Genes in Papoviruses

A

Following replication, late transcription of the capsid
genes occurs.
• Capsid proteins self-assemble and package the
viral DNA. Cell lysis occurs, and viral particles are released.
• Large T-antigen is a multifunctional protein and
also binds to and inactivates tumor suppressor genes Rb and p53. This overcomes cell growth inhibition leading to tumor development.
• Large T-antigen is essential for virus replication
and tumor development.

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20
Q

Human Papilloma Virus

A

The most important member of papovavirus family
is human papillomavirus (HPV). HPV is responsible for benign tumors, called papillomas, including plantar and genital warts (condylomata acuminata). Certain types are strongly associated with the development of cervical carcinoma. There is also an association with head and neck
cancers.
Of the >60 different HPV types about 1/3 are associated with anogenital lesions. Approximately one third of college aged women harbor HPV in their cervix.

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21
Q

Human Papilloma Virus

Epidemiology

A

Early epidemiological studies of cervical neoplasia
suggested a direct causal relationship with sexual activity (multiple partners or early onset of sexual relations). A second risk factor exposure to a promiscuous male. Molecular analysis has indicated that 80-90% of cervical carcinomas
harbor HPV viral sequences integrated into the cellular DNA. HPV is considered the etiologic agent of invasive cervical carcinoma.

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22
Q

Human Papilloma Virus

Clinical Manifestation

A

The most common manifestations of urogenital
HPV infection are condylomas. Most condylomas are caused by nononcogenic type of HPV (6b and 11).
Greater than 75% of cervical carcinomas are caused by two high risk papillomaviruses, HPV16 and HPV18.

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23
Q

HPV Oncogenes

A

Two HPV oncogenes have been identified, the

early genes E6 and E7, which are also essential for viral growth.

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24
Q

E6 and E7

A

In warts the viral genome is extrachromosomal
(not integrated) and the virus replicates. In cervical tumors cells the E6 and E7 oncogenes are found integrated into the cellular chromosome and are highly expressed.
E6 binds to p53 and E7 binds Rb, thus inactivating
these tumor suppressors and allowing entry to the cell cycle, leading to transformation.

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25
Q

Other Factors associated with HPV

A 
Other cofactors (smoking cigarettes for one) are
involved in the generation of cervical carcinoma since woman infected with HPV 16 or 18 do not always develop cervical cancer.
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26
Q

Cervical cancer Prevention

A

Current clinical strategy for prevention of cervical
cancer is based on encouraging “safe sexual” practices and early detection of abnormal cells by yearly cytologic examination of cervical smears (Papanicolaou stain).

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27
Q

HPV Vaccine

A

A recombinant vaccine has been developed and
is now licensed for pediatric use. It is based on viral
capsid proteins expressed in yeast.
• Gardisil: Protects against HPV 16/18 and HPVs 6 and 11
• Cervarix: Protects gainst HPV 16/18 only

Results on cervical cancer will be seen in about 20 years

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28
Q

Adenovirus

A

Although adenoviruses are not associated
with tumors in humans, some can cause tumors
in hamsters and transform rat cells in vitro

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29
Q

Adenovirus

Tumor genes

A

Two proteins are associated with transformation:
• E1A that can partially transform cells on it’s
own, and
• E1B that does not transform but increases
levels of E1A.

30
Q

Adenovirus

E1

A

E1 binds to the tumor suppressor proteins Rb, p300 and CBP. It also binds to cellular transcription factors to stimulate transcription associated with S phase where DNA replication occurs.

31
Q

Herpes Virus

A

Herpesviruses have a large, linear double stranded DNA genome, with an icosahedral nucleocapsid, surrounded by a protein tegument, enclosed in a glycoprotein bearing envelope.

32
Q

Herpes Virus

That cause Cancer

A

Two herpesviruses are known to cause cancer:
• Epstein Barr virus causes Burkitt’s lymphoma,
• Kaposi’s sarcoma herpes virus (HHV8) is a virus isolated from AIDS patients that causes Kaposi’s sarcoma.

Tumors associated with these viruses are normally a consequence of LATENT infection with the virus, usually years after the primary infection.

33
Q

Epstein-Barr Virus

A

• Burkitt’s lymphoma is the most frequent childhood
tumor in Africa. Boys are at greater risk.
• Tumors are multifocal, malignant B-cell lymphomas, which often present as large masses in the jaw or lower abdomen. Histologically tumors have a “starry cell” appearance. If untreated, patients generally die within 6 months of diagnosis. Chemotherapy works.
• While the lymphoma is prevalent in certain regions
of Africa, it is very rare in the Europe and the US.

34
Q

EB Virus Discovery

A

• EB virus was discovered by Denis Burkitt during
his efforts to identify the cause of lymphoma in African children.
Burkitt noticed that the geographical distribution of
the tumor was limited to equatorial Africa, and was set by rainfall and temperature. The fact that the tumor was only seen in hot, wet regions (as was yellow fever) led him to propose that a tumor virus with a mosquito vector was responsible.
Burkitt was correct about the viral etiology, but
wrong about a mosquito vector.
• Epstein and Barr, and others later established lymphoma tissue culture cell lines from patients. These cell lines contained viral particles similar to herpesvirus. EB virus is also found in B-cells from patients with infectious mononucleosis.

35
Q

EB Virus Infection Markers

A

The presence of transformed, latently infected Bcells cells is a biological hallmark of EB virus infection.
Transformed B-cells always contain extrachromosomal EB virus genomes, however, no virus is produced. Integration of viral genes is NOT required for cell transformation.

36
Q

EB Virus -Burkitt’s Lymphoma

Genetics

A

Burkitt’s lymphoma tumors have a chromosomal
translocation between chromosome 8, and chromosome 14 or chromosome 22; t(8;14) and t(8:22). Either translocation places the c-myc proto-oncogene on chromosome 8 under transcriptional control of an immunoglobin gene.
This causes the proto-oncogene to be overexpressed and causes immortalization.

37
Q

EB Virus

Cell Transformation

A

EBV transforms cells through the co-ordinate expression of five viral genes, which include EBNA-2, a transcriptional activator particularly for genes involved in the NOTCH pathway, and LMP-1, a functional homologue of CD40.

38
Q

EB Virus

Immune Response

A

Ordinarily the immune system contains these
transformed cells by an aggressive T cell response. Only when the immune response is compromised does do these cells grow as tumors.

39
Q

EB Virus

Effects of Malaria

A

Infection with malarial parasites is thought to play
a role in disease development which accounts for the restricted geographic distribution of Burkitt’s lymphoma. Malaria is a cofactor because it inhibits cell-mediated immunity in children.

40
Q

EB Virus

Nasopharyngeal carcinoma

A

EB virus also infects epithelial cells, and is highly
associated with nasopharyngeal carcinoma. This occurs with a high incidence (98/100,000) in older males in southern China and Southeast Asia. The molecular basis of transformation of epithelial cells is not understood.

41
Q

EB Virus

Other Complications

A

EB virus also causes post-transplant lymphoproliferative disease in immunosuppressed graft recipients. It has also been associated with several other malignancies such as gastric carcinoma, Hodgkin’s disease, and tumors seen in AIDS patients (CNS lymphomas, non-Hodgkin’s
lymphoma).

42
Q

Kapsoi’s Sarcomaassociated Herpesvirus (KSHV)

A

• AIDS-associated Kaposi’s sarcoma (KS) is the
most frequent neoplasm occurring in persons with AIDS. 15 - 20% of AIDS patient develop KS.
• KSHV, also called HHV8, has been found in virtually all biopsies of AIDS associated Kaposi’s sarcomas.
• Prior to the 1980s KS was clinically rare and observed mostly in elderly males of Mediterranean or eastern European descent.

43
Q

Kapsoi’s Sarcomaassociated Herpesvirus (KSHV)

Tumors

A

• Tumors usually present as multiple, pigmented,
highly vascularized nodules of the skin. Tumors contain replicating spindle cells.
• Tumor cells express high levels of a powerful angiogenic factor, called vascular endothelial growth factor (VEGF). This is a CELLULAR protein, not from the virus.

44
Q

Kapsoi’s Sarcomaassociated Herpesvirus (KSHV)

Oncogenes

A

Several viral genes are believed to be oncogenes.
One called, G-protein coupled receptor (GPCR) induces VEGF expression and angiogenesis. There is also a virally-encoded cyclin homolog and the LANA antigen has been shown to activate cellular genes promoting cell growth.

45
Q

Retroviruses

A

Retroviruses are enveloped viruses with a nucleocapsid containing two identical copies of positive sense, single-stranded RNA about 10 kilobases long.

46
Q

Retroviruses

Genes

A

All nondefective retroviruses encode three essential
genes: gag, pol and env.
• gag -encodes nucleocapsid and capsid proteins.
• pol - encodes reverse transcriptase and integrase.
• env -encodes envelop glycoproteins.

47
Q

Retroviruses Classification

A

Medically important retroviruses fall into two subfamilies:
• Oncoviruses, which are associated with tumor formation - Rous sarcoma virus (RSV), feline leukemia virus (FeLV), avian leukosis virus (ALV), murine leukemia virus (MuLV), human Tcell
leukemia virus-1 and 2 (HTLV-1,-2), and others.
• Lentiviruses, which are not directly associated with tumor formation - human immunodeficiency virus-1 and 2 (HIV-1,-2).

48
Q

Retroviruses

Life Cycle

A

Retroviruses have two phases in their life cycle:
• An extracellular phase as a viral particle. Retroviral
virions have a single-stranded RNA genome.
• An intracellular phase as a provirus. A provirus is a double-stranded DNA copy of the retroviral genome integrated into the host cell chromosome. Viral replication and transcription occur from the provirus.

49
Q

Retroviruses

Inhibitors and Replication

A

Unlike other plus strand RNA viruses, retroviral replication is blocked by inhibitors that specifically block DNA synthesis.This finding first led to the proposal that retroviruses replicate from a DNA intermediate.

50
Q

Retroviruses

Replication

A
  • When a retrovirus infects a cell the virion RNA is copied into double-stranded DNA by a viral protein called reverse transcriptase. Reverse transcriptase is an RNA-directed DNA polymerase.
  • The sequence of the DNA provirus is the same as the RNA genome in viral particles except for the very 5’ and 3’ ends which become duplicated during reverse transcription, and are called Long Terminal Repeats (LTR). The LTRs contain regulatory elements for viral transcription. Genome replication and mRNA transcription occurs from the DNA provirus.
51
Q

Retrovirus Replication

Steps

A
  1. The retrovirus adsorbs to the host cell plasma membrane. The viral envelope fuses with the plasma membrane and the nucleocapsid is released into the cytoplasm. Reverse transcriptase is bound to the nucleocapsid.
  2. Next, the single-stranded viral RNA is copied into doublestranded DNA by the reverse transcriptase. Reverse transcription begins at a primer of cellular tRNA. The initial product is a DNA-RNA hybrid. A ribonuclease specific for DNA-RNA hybrids (RNase H, another activity of reverse transcriptase) degrades the viral RNA. Finally, reverse transcriptase synthesizes the second DNA strand. The double-stranded DNA genome is slightly longer than the initial viral RNA because during reverse transcription Long Terminal Repeats (LTRs) sequences are added to each end.
  3. The newly synthesized double-stranded DNA is released from the nucleocapsid, enters the nucleus, and integrates at a random site in the cellular DNA. The viral protein integrase catalyses this process. The LTRs are important in integration. Once integrated, it is called a provirus.
  4. The integrated provirus is transcribed and replicated by the host messenger RNA polymerase, and utilizes transcriptional regulatory elements in the LTR. mRNA transcripts are capped and polyadenylated in the same fashion as all cellular mRNAs.
  5. The RNA transcripts have two fates. Initially, they are spliced, and exported to the cytoplasm and translated into the viral proteins.
  6. Later, full length RNA genomes are packaged into nucleocapsids.
  7. Nucleocapsids bud through the cytoplasmic membrane for final assembly into mature, enveloped viral particles
52
Q

Classification of Oncogenic Retroviruses

A

Retroviruses rarely cause cancer in humans. Most oncogenic retroviruses infect rodent or avian species.
Oncogenic retroviruses can be categorized into:
• Acute transforming viruses - cause cancer rapidly in laboratory animals, and quickly transform tissue culture cells. These viruses have an oncogene. In most cases, the oncogene replaces one of the normal viral genes (gag, pol, and env), and so they are defective.
• Nonacute transforming retroviruses - take many
years to cause cancer in laboratory animals. These viruses do not have oncogene.

53
Q

Classification of Oncogenic Retroviruses

Based on appearance

A

The oncogenic retroviruses are also classified into different types (A,B,C,D) based on their appearance under the electron microscope.

54
Q

Transforming Retroviruses

A

Transforming Retroviruses have in 3 basic flavors:
• Transducing
• Non-transducing
• Non-transducing, long latency

55
Q

Acute transforming viruses

A

• The acute transforming virus, Rous sarcoma virus
(RSV), induces sarcoma rapidly in chickens
(within weeks to a few months) and transforms tissue culture cells soon after infection (24 hours).
• RSV and carries a viral oncogene, called src .
The src oncogene gene was identified using transformation defective mutants of RSV that contained a deletion in the viral genome.
• The expression of src is required for both the induction and maintenance of the transformed phenotype.

56
Q

Rous sarcoma Virus and the Discovery of Proto-oncogenes

A
  • Experiments utilizing a radioactive copy of the src gene showed that this probe hybridized to DNA from normal chicken cells, indicating that normal cells have a gene homologous to the viral gene.
  • The cellular copy is called a proto-oncogene, and the viral oncogene is derived from it. It is thought that during evolution the acute transforming retroviruses incorporated copies of proto-oncogene into their genomes.
  • The src gene encodes a tyrosine specific protein kinase.
  • The viral src gene is mutated relative to the cellular protooncogene, and the oncoprotein has a 50-100-fold higher kinase activity than the normal Src protein.
57
Q

Proto-oncogenes

A

Using probes made from the viral oncogenes of
other acute transforming viruses more 30 protooncogenes
have been identified. They all play important
roles in growth regulation and can be divided into 5
groups:
1. growth factors
2. growth factor receptors
3. protein kinases
4. signal transducing G-proteins
5. nuclear proteins that regulate transcription, and DNA replication.

58
Q

Proto-oncogenes

Growth Control

A

Proto-oncogenes are positive growth control
switches. Think of the proto-oncogenes as “GO SIGNALS”. In normal cells proto-oncogenes do not cause cancer. Rather, they regulate growth and cellular differentiation. If proto-oncogenes are mutated or expressed at abnormally high levels they become oncogenes and the tightly regulated networks that control cellular growth are short-circuited. This leads to cancer.

59
Q

Defective Retroviruses

A

All of the known acute transforming retrovirus, except one, has one or more of the viral gene required for growth (gag, pol, or env) replaced by an oncogene.
They are called Defective Retroviruses.
For example, in the acute transforming virus
MC29, which cause myelocytomas, the pol and env
genes have been replaced by the myc oncogene.
Defective, acute transforming retroviruses can
not produce infectious virions unless the cell is also
infected with a related nondefective retrovirus,
called a “helper virus”, which supplies the missing
viral proteins. Therefore, all isolates of a defective virus willbe mixtures that contain both the defective virus and helper virus.

60
Q

Why Oncogenes of Acute Transforming Retroviruses Cause Cancer

A

• When an acute transforming virus infects a cell,
the RNA genome containing an oncogene is reverse transcribed into DNA that integrates in the cellular chromosome. Transcription from the retroviral promoter is very active since the retrovirus needs to make viral mRNA for replication and translation. Therefore, the viral oncogene is also expressed at very high levels disrupting cellular growth control.
• Viral oncogenes frequently have mutations relative
to their normal cellular counterparts, which causes
them to have increased activity. In the case of the viral src gene, mutations cause the viral Src protein to have an elevated protein kinase activity relative to the cellular Src protein which contributes to the oncogenic activity of the viral gene.

61
Q

Nonacute Transforming Retroviruses

A

• Retroviruses in this class:
a. do not have a viral oncogene
b. are nondefective and replicate by themselves without a helper virus.
c. take a long time to induce cancer (many months
or years).
• In tumors caused by nonacute transforming retroviruses the provirus is often found integrated adjacent to a proto-oncogene. This is a rare event and often takes years.
• This places the proto-oncogene under the control
of the highly active retroviral promoter (transcriptional control region in the LTR), and causes increased protooncogene expression. This is called insertional activation of proto-oncogenes, and it is a low probability event explaining why it takes many years following infection for tumors to appear.

62
Q

Nonacute Transforming Retroviruses

Insertional activation of proto-oncogene expression by a nondefective retrovirus

A

Insertional activation of proto-oncogene expression by a nondefective retrovirus. Many years following infection by a nondefective retrovirus insertion may occur in front of a cellular proto-oncogene. Since the viral transcriptional regulatory elements are very active this can result in overexpression of the proto-oncogene and lead to tumor formation.

63
Q

Non Transducing Retroviruses

A
  • Replication competent
  • Insertional activation of cellular proto-oncogene
  • Slower Transformation
  • Rarely see insertional activation of tumor supressors
64
Q

Human Retroviruses

A
  • The only oncogenic human retroviruses are human T-cell leukemia virus-1 and 2 (HTLV-1,2).
  • HTLV-1 is the etiologic agent of adult T-cell leukemia (ATL).
  • It is endemic in southern Japan, central Africa and the Caribbean. Incidence of infection in US is 0.025%.
  • HTLV-1 and 2 appear to be transmitted horizontally via sexual contact or in blood or breast milk.
  • Infected individuals are usually asymptomatic.
  • Approximately 0.1% of infected individuals develop adult Tcell leukemia following a long latency of 10 - 30 years.
  • Viral tax protein is a transcription factor and induces IL-2 and it’s receptor and may set up an autocrine loop, predisposing to transformation.
65
Q

Heptatitis B

A
  • Hepatitis B virus causes primary hepatocellular carcinoma the leading cause of cancer deaths worldwide. Hepatitis B virus is responsible for 500,000 cancer deaths annually.
  • About 5% percentage of infected individuals become chronic carriers and express virus for life. 2-4% of these carriers goes on to develop primary hepatocellular carcinoma.
66
Q

Heptatitis B

Tumorigenesis

A

• Tumors have integrated of hepatitis B virus DNA. Mechanism of tumor induction is unclear and likely very complex. It is suspected that in some cases integration near a cellular proto-oncogene leads to overexpression and induces transformation.
Some viral proteins may also act as oncogenes, but
this has not been conclusively shown.
• Another important mechanism likely involved in tumorogenesis is constant destruction of liver tissue by the immune response, followed by regeneration, which may predispose to mutations leading to cell transformation.

67
Q

Heptatitis B

Immunization

A

Immunization against hepatitis B virus may help prevent primary hepatocellular carcinoma, particularly in the case of maternal transmission to neonates.

68
Q

Heptatitis B

Replication

A

Hepadnavirus replication is similar to retroviral replication in that it utilizes hepadnavirus reverse transcriptase.

69
Q

Retroviruses and Hepatitis B virus

A

The most important concept is that both retroviruses and hepatitis B virus depend on reverse transcriptase that is found in the virion. In the retroviruses, the reverse transcription event takes
place as a very early event in the infection of a cell. In hepatitis B virus the reverse transcription event takes place very late in production of virions. Recall the reverse transcriptase of hepatitis B can be inhibited by lamuvidine, the same drug used to inhibit retroviral reverse transcriptase.

70
Q

Hepatitis C

RNA virus – Flavivirus

A

• Recall that the majority of patients infected with
HCV become persistently infected, and 20% will
develop life-threatening cirrosis and some develop
life-threatening hepatocellular carcinoma.
• Some viral proteins may have oncogenic activity,
but it has no been proven conclusively.
• The virus does not integrate into the genome.
• Infection by the virus itself does not kill liver cells,
but the immune response to infection likely promotes tumor development.
• As for HBV, alcoholism greatly enhances the rate of hepatocellular carcinoma, suggesting constant
liver damage and regeneration predisposes towards
mutations and cancer development.

Virology Quiz 4 (6 decks)

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