Viruses Part 2 Test Answers – Flashcards

Animal viruses multiply differently from bacteriophages based on their mode of entry into host cells, biosynthesis, and release 1. Attachment 2. Penetration/Entry 3. Uncoating 4. Biosynthesis a. DNA-containing Viruses b. RNA-containing Viruses 5. Maturation 6. Release

- Animal viruses attach to the proteins and glycoproteins(receptor) of the plasma membrane of the host cell. - Receptor sites are inherited characteristics of the host, thus the receptor for a particular virus can vary from person to person. - This could account for individual differences in susceptibility to a particular virus. - Ex. People who lack the CD4 receptor & CCR5 coreceptor for HIV do not acquire AIDS

- In non-enveloped animal viruses, penetration occurs by endocytosis (i.e. pinocytosis). - The virion is enclosed within the vesicle and is then transported into the host's cytoplasm. - For enveloped viruses, the viral envelope fuses with the host's plasma membrane and the capsid is released into the host's cytoplasm (fusion)

- Uncoating only occurs in animal viruses. - Uncoating is the separation of the viral nucleic acid from its protein coat once the virion is in the vesicle. - The viral nucleic acid is then released into the cytoplasm of the host cell. - Some animal viruses have viral coded enzymes to uncoat Ex: Poxviruses - Other animal viruses are uncoated by enzymes (lysozyme) in the host cell. Ex: Herpes simplex virus and poliovirus

- the biosynthesis of viral nucleic acid and capsid differ depending on the type of viral nucleic acid A. Biosynthesis for DNA-Containing Viruses: - In general: 1. DNA-containing viruses (parvoviruses, papovaviruses, adenoviruses, and herpesviruses) replicate their DNA in the nucleus of the host cell 2. viral protein is synthesized in the cytoplasm 3. the proteins then migrate into the nucleus of the host cell, and there, they are assembled into complete viruses. - Exception: Poxviral components are synthesized and assembled in the cytoplasm of the host cell. Process of DNA virus multiplication (i.e. papovavirus): 1. After attachment, penetration, and uncoating, the viral DNA is released into the nucleus of the host cell. 2. A portion of the viral DNA (early genes) is transcribed into mRNA and then translated into enzymes needed for multiplication of viral DNA. 3. After the initiation of DNA multiplication, transcription and translation of the remaining "late" viral genes occur: capsid & other structural proteins are synthesized in the cytoplasm. 4. The capsid proteins migrate into the nucleus of the host cell and the assembly of the viruses is completed (maturation).

- Multiplication of RNA viruses takes place in the host cell's cytoplasm. - Process of biosynthesis differs between the different RNA viruses 1. Ex. Picornavirus — sense (+) strand RNA virus - After attachment, penetration, and uncoating are completed, the sense RNA (like mRNA) is translated into 2 principal proteins. - One protein inhibits the host cell's synthesis of RNA and protein - The other protein is the RNA-dependent RNA polymerase (RdRP) synthesizes a complementary strand (antisense RNA) from the sense (+) RNA strand. - The antisense strand can serve as a template to produce additional + strands using RdRP. - The + RNA strand (act as mRNA) is used for translation of capsid proteins and nucleic acid for new virions. - Viral RNA and viral capsid are then assembled into complete viruses during maturation stage 2. Ex. Rhabdovirus - antisense (-) strand RNA virus - such as the rabies virus -They contain viral RNA-dependent RNA polymerase that uses the (-) strand as a template to produce a (+) RNA strand (mRNA like). - (+) strand then serves as the mRNA for synthesis of viral proteins (capsid) and as the template for synthesis of new viral (-) RNA - antisense (-) RNA strand are then incorporated into capsid during maturation stage 3. Reovirus - dsRNA virus - are found in the respiratory and enteric (digestive) systems of humans. - REO comes from Respiratory, Enteric, and Orphan (viruses not associated with any diseases). - are usually not pathogenic - After the capsid containing the double-stranded RNA enters a host cell, mRNA (+ strand) is produced. - mRNA is used as template to synthesize more viral proteins and (-) strand RNA - One of the new proteins is an RNA-dependent RNA polymerase, which produces more (-) strand of RNA. - The mRNA (+) and (-) strands form the double stranded RNA that is then surrounded by capsid proteins. 4. Retrovirus - includes genera Lentivirus (HIV) and Oncovirus - includes the human immunodeficiency viruses (HIV- and HIV-2), which cause AIDS; envelope virus - contains 2 identical (+) strand RNA molecules - retroviruses carry its own reverse transcriptase enzyme to synthesize complementary dsDNA using RNA as the template - viral RNA is also degraded by the reverse transcriptase - viral integrase enzyme then joins/integrates the viral DNA with the host's chromosome — viral DNA referred tp as provirus - provirus is protected from host's immune system and antiviral drugs - In the latent state, provirus DNA replicates each time the host cell divides/replicates - In the active state, provirus can express its genes and produce new viruses to infect neighboring cells - mutagens such as gamma radiation can induce expression of provirus. - retroviruses are released from the host cell via budding

- 1st step of viral maturation is the assembly of the capsid protein (this is usually spontaneous). - Viruses which have envelopes (such as myxoviruses and paramyxoviruses) synthesize the viral envelope protein and incorporate the protein into the plasma membrane of the host cell. - The envelope's lipid and carbohydrate are synthesized by host cell enzymes and are present in the plasma membrane. - The envelope develops around the capsid, which contains the nucleic acid, as the virus pushes out of the cell by a process called BUDDING - Budding does not immediately kill the host cell and in some cases the host cell survives. - Nonenveloped viruses are released through rupture of the host cell membrane. - This results in the death of the host cell

penetration occurs by endocytosis (i.e. pinocytosis). - The virion is enclosed within the vesicle and is then transported into the host's cytoplasm

the viral envelope fuses with the host's plasma membrane and the capsid is released into the host's cytoplasm (fusion)

People who lack the CD4 receptor & CCR5 coreceptor for HIV do not acquire AIDS

cytoplasm

early viral genes are the genes required for the synthesis of enzymes needed for the multiplication of viral DNA late viral genes are genes required for the synthesis of the capsid and other structural proteins synthesized in the cytoplasm

Animal viruses attach to the proteins and glycoproteins(receptor) of the plasma membrane of the host cell Receptor sites are inherited characteristics of the host, thus the receptor for a particular virus can vary from person to person

synthesizes a complementary strand (antisense RNA) from the sense (+) RNA strand

enzyme that can synthesize complementary dsDNA using RNA as the template

a virus genome that is integrated into the DNA of a host cell.

a bacteriophage (often shortened to "phage") genome inserted and integrated into the circular bacterial DNA chromosome or existing as an extrachromosomal plasmid. This is a latent form of a phage, in which the viral genes are present in the bacterium without causing disruption of the bacterial cell.

Nonenveloped viruses are released through rupture of the host cell membrane. - This results in the death of the host cell

The envelope develops around the capsid, which contains the nucleic acid, as the virus pushes out of the cell by a process called BUDDING - Budding does not immediately kill the host cell and in some cases the host cell survives.

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The relationship between cancers and viruses was first demonstrated in 1908 when Wilhelm Ellerman and Olaf Bang found that leukemia could be transferred to healthy chickens by viruses

found that a chicken sarcoma (cancer of connective tissue) can be transmitted by viruses

cancer of glandular epithelial tissue

In 1972, a human cancer-causing virus was discovered & isolated by Sarah Stewart.

Oncogenes were first identified in cancer-causing viruses and Michael Bishop and Harold Varmus received the 1989 Novel Prize in Medicine for proving that the oncogenes in viruses are derived from animal cells

Oncogenes are proto-oncogenes (i.e. growth factors, proliferation, etc.) that gains a function when mutated A proto-oncogene is a normal gene that can become an oncogene due to mutations or increased expression

Oncogenic viruses or oncoviruses are viruses that cause tumors in animals. All oncogenic viruses integrate their DNA into the host's chromosome and replicates as the host cell reproduces - Not all viruses that are able to integrate into the host's genome cause cancer; virus-induced cancer does not appear to be contagious - Tumor cells are transformed cells

Burkitt's lymphoma and nasopharyngeal carcinoma

Papilloma viruses

Hepatitis B virus (HBV)

Human T cell Leukemia viruses (HTLV 1 and HTLV 2) are retroviruses that are associated with leukemia and lymphoma in humans

sarcoma - cancer originating from connective tissue

Leukemia in cats and is transmissible between cats

A virus can remain in the host cell and not actually produce disease for a long period, often many years, the virus can be reactivated by immunosuppression or byother chemical signals Ex. 1: The varicella-zoster virus (herpes zoster virus) causes chickenpox (varicella) & can also exist in a latent state. If the virus enters neurons and become latent, it can be reactivated in response to changes in the immune response to cause Shingles (zoster).

refers to a disease process that occurs gradually over a long period of time - Typically, slow viral infections are fatal. - Persistent or chronic viral infections differ from latent viral infection in that the persistent viral infection exhibits gradually increasing numbers of infectious virus over a long period rather than appearing suddenly. Ex. Hepatitis B virus can cause increased cell growth at first, but can gradually cause liver cancer if it becomes a persistent viral infection

A latent viral infection can be present but not cause any symptoms of disease for long periods of time and remain undetected whereas a persistent viral infection causes a disease that slowly but surely produces symptoms and is noticeably present

benign and malignant tumors

consist of cells which simply divide, but do not break through the basement membrane

cells proliferate and can break through the basement membrane to invade neighboring tissues --> metastasis Carcinomas: tumors originating from epithelial tissues (e.g., glands, skin, lung epithelium) Sarcoma: tumors originating from connective

tumors of the glandular tissue of the breast or intestinal tract (benign)

tumors of the musculature (benign)

tumors of the glia cells (benign)

tumors originating from epithelial tissues (e.g., glands, skin, lung epithelium) (malignant)

tumors originating from connective (malignant)

1. immortal 2. rapid cell cycle 3. loss of contact inhibition High motility Express high levels of membrane proteins Express high levels of growth factors

a. involved in promoting cell proliferation and migration b. Encode growth factors or other signaling molecules c. Growth factor recpetors d. Intracellular molecules e. A proto-oncogene that gains a function when mutated is called an oncogene

a. Involved in inhibiting/suppressing cell proliferation and migration b. Encode proteins controlling cell cycle c. Cytoskeletal molecules d. Adhesion molecules e. Recessive, loss of function results in carcinogenic effect

P53: transcription factor --> functions to stop cell division if cell contains damaged DNA and promotes cell death (apoptosis) for the damaged cell • p53 mutation leads to a rapidly growing clone of cells with multiple chromosomal abnormalities. Major fraction of all malignant tumor cells exhibit p53 mutations