10A. Lecture

Question 1

aborting infection

Answer 1

no virus release

Question 2

productive invfection

Answer 2

virus release and shedding

Question 3

resistance of host

Answer 3

•No surface receptor for viral attachment

→ Not susceptible ~ host spectrum

Question 4

(IFN) interferon

Answer 4

cell-coded mediator protein - cellular defence mechanism

Question 5

IFN production

Answer 5

Interferon inducer: dsRNA, RI forms  cascade – IFN release

Question 6

IFN effects

Answer 6

IFN effects: on the neighbouring cell!
- structural changes on the cytoplasmic membrane
→ penetration
- L-RNase: mRNA degradation
- proteinkinase: protein production inhibited

Question 7

IFN types

Answer 7

heat and pH resistance, viral induction:
- IFN- (epithel, leucocytes)
- IFN- (fibroblast)
antigen, mitogen induces:
- IFN- (lymphocyte)

Question 8

IFN efficancy and production rate

Answer 8

•IFN efficacy: 10-9 mg dose
•Production:
- 2-4 h after infection
- maximum after 12 h
- clearance after 24 h

Question 9

specificity of IFNs

Answer 9

• Not virus specific

* Host specificity

Question 10

IFN therapy problems

Answer 10

• expensive
• parenteral use, short-term efficacy
• the inducers (poly-inozine, poly-cytidine) are toxic
• toxic side effects

Question 11

latency of viruses

Answer 11

• After infection the virus does not multiplicate
→ balance with the cell
• Only the nucleic acid and early proteins are present
• episoma (Papilloma-, Herpesviridae)
• integration – provirus (Retro-, Polyomaviridae)
• No virus shedding, no clinical signs, but carrier!
• Reactivation
• immunosuppression
→ shedding, clinical signs

Question 12

Persistent infection of viruses

Answer 12

•Virus production, but not severe cell damage
→ Continuous shedding
•In vitro cell cultures: diagnostic problems

Question 13

oncogenic effect of viruses

Answer 13

leads to tumor production
•cell proliferation
•less differentiated cell forms („ancient”)
•less effective cell forms
•usually not able to function effectively
→ Tumors

Question 14

cellular oncogenesis

Answer 14

lead to tumor production
•oncogenes (even 5% of the genome)
•genes necessary for cell division and maturation
•in the active cell suppressed proto-oncogenes (c-onc)
•activation – oncogenesis

Question 15

•Oncogenic viruses:

Answer 15

DNA viruses: Papilloma-, Polyoma-, Adeno-, Herpes-,
Pox-, Hepadnaviridae
RNA viruses: Retroviridae

Question 16

tumor types

Answer 16

• Benignant: limited, less invasive, less destructive

* Malignant: invasive, destructive

Question 17

Activation of cellular oncogenes

Answer 17

•Retroviridae (Avian leukosis virus, Feline leukosis virus)
•DNA integration into the cellular genome
•near-by c-onc genes
•retroviral LTR regions → intensive promoter – translation
→ c-onc activated – oncoprotein expression – cell proliferation
→ slow developing lymphatic tumors (leukemias)

Question 18

Expression of viral oncogenes

Answer 18

Retroviridae
•recombination between the cellular and pro-viral genome
•transposition of the c-onc gene into the virus genome
→ v-onc!
•the oncogene is carried by the virion
•after infection quick onco-protein production
•fast developing malignant tumors (sarcoma, carcinoma)
•the v-onc gene is not essential for the virus
•replacing essential genes (envelope protein gene)
•defective particles – envelope from leukosis virus

Question 19

Viral proteins with consequent oncogenic effect

Answer 19

• oncogenic DNA viruses
• viral modulator proteins control the cell machinery
• inactivation of cellular anti-oncogenic proteins
• inhibition of the apoptosis (Adenoviridae)
• usually benignant tumors

Question 20

•In vitro cell cultures

Answer 20

malignant transformation

•contact inhibition is terminated: microtumors