Virology Viva Answer
Virology Viva Answer
Virology Viva Answer
Virology
1. Tell the feature of a virus.
Features of virus:
1) Viruses are the smallest microscopic organism.
2) Obligate intracellular parasite.
3) Contain either DNA or RNA but not both.
4) They are acellular organisms.
5) All viruses do not have enzymes for energy metabolism.
6) They can not synthesize protein due to absence of ribosome.
7) Viruses are generally resistant to antibiotics.
8) Viruses are sensitive to interferon.
9) Viruses are found in plants, animals and bacteria.
10) Viruses are transmissible.
11) Isolation and identification of viruses can be done by living tissue culture.
12) Can not be culture in artificial media.
Virus
No (Acellular)
0.02-0.2 m
Bacteria
Yes (Cellular)
1-5 m
4)
5)
6)
7)
Parvo virus
HIV
Cytomegalo virus
Hepatitis B & C virus
Hepatitis A Virus
Hepatitis B Virus
Hepatitis C Virus
Hepatitis D Virus
Hepatitis E Virus
Other hepatitis Virus: (Mnemonic: CHERY-A)
a. Cytomegalo virus
b. Herpes virus
c. Epstein Barr Virus
d. Rubella virus
e. Yellow Fever Virus
f. Adeno Virus
19. Name hepatitis viruses that can be transmitted through blood & blood product.
Hepatitis viruses that transmit through Blood and Blood Products:[Mnemonic: Consonants- BCD out of
Hepatitis ABCDE]
a) Hepatitis B virus
b) Hepatitis C virus
c) Hepatitis D virus
Hepatitis Viruses that transmit through Faeco-oral route: [Mnemonic: Vowels- AE out of Hepatitis
ABCDE]
a) Hepatitis A virus
b) Hepatitis E virus
20. Name hepatitis viruss that have chronic carrier state.
Hepatitis Viruses that have chronic carrier state:[ Mnemonic: Consonant: BCD]
a) Hepatitis B virus
b) Hepatitis C virus
c) Hepatitis D virus
21. Mode of transmission of HAV
Transmission of HAV (Hepatitis A Virus):
[In short]: Faeco-oral route
26. Name the antigens present in HBV virion. Mention their importance.
Antigens present in HBV virion:
1) HBsAg
2) HBcAg
3) HBeAg
[ N:B: Detection of Ag in serum: HBsAg, HBeAg ]
Importance:
1) HBsAg: is the indication of recent or chronic infection (If >6 month = carrier state)
2) HBeAg: is the indication of replication stage of virus and the patient is highly infectious.
27. What are the serological markers of hepatitis B infection?
Serological markers of hepatitis B virus infection:
A. Detection of Ag in the serum:
a. HBsAg
b. HBeAg
B. Detection of Ab in serum:
a. Anti HBcIgM
b. Anti HBsIgG [mnemonic: sG= Singapore]
c. Anti HBcIgM
Importance:
1) Detection of HBsAg is the indication of recent or chronic infection. (If > 6 months = carrier state)
2) Detection of HBeAg is the indication of replication stage of virus and the patient is highly infectious.
3) Detection of HBcIgM is the most reliable test for active hepatitis B infection. ( Recent and in
window period)
4) Detection of Anti HBsIgG indicates protective immunity against HBV infection ( life long
immunity)/ vaccination/ post infection/ passive immunity.
5) Detection of Anti HBeIgM, indicates recovery & low transmissibility.
28. Give interpretation:
1) HBsAg +ve
2) Total anti-HBc positive
3) IgM anti-HBc negative
Interpretation:
Chronic hepatitis
29. Give interpretation:
1) HBsAg (-)ve, Anti-HBs (+)ve
2) HBsAg (-)ve, Anti HBs (+)ve, Anti HBc (+)ve
Interpretation:
1) Post infection/ vaccination
2) Window period
30. What is window period in case of hepatitis B? How can you diagnose acute hepatitis B in this period?
Window period:
During infection by HBV, there is a period of several weeks, then HBsAg has disappeared but
HBsAg is not yet detectable. This period is called window phase/ window period. In this time IgM of Anti
HBc Ab is always positive and can be used for diagnosis.
Diagnosis of Acute hepatitis B in window period:
Serological test: Anti HBc IgM is always positive in window period.
31. How can you diagnose acute hepatitis B?
Diagnosis of Acute hepatitis B:
Detection of HBsAg in the serum:
If HBsAg (+)ve it indicate acute or chronic HBV infection.
If HBsAg ()ve, we will do, Anti HBcIgM in the serum, If Anti HBcIgM (+)ve it indicate the
window period of hepatitis B infection.
32. Mention outcomes of hepatitis B virus infection?
Outcome of hepatitis B virus infection: [Ref: Lange]
1) Subclinical infection Recovery
2) Acute hepatitis
a. Recovery
b. Fulminant hepatitis Death
3) Chronic carrier:
a. Asymptomatic/ healthy carrier
b. Chronic active hepatitis leads to cirrhosis and death.
33. Mode of transmission of hepatitis C virus (HCV).
Mode of transmission (Routes) of hepatitis C virus:
1) Blood transmission
2) Contaminated syringes and needles (drug abusers)
3) Needle stick injury
4) Sexual transmission
5) From mother to child (Prenatal through placenta, during delivery in birth canal, post natal)
[Ref: Lange]
34. What are the possible outcomes of HCV infection?
Possible outcomes of HCV infection: (Complications)
1) Chronic hepatitis/CLD
2) Cirrhosis of liver
3) Fulminant hepatitis (Rare)
4) Hepatocellular carcinoma
5) Death
35. How can you diagnose an acute HCV infection in the laboratory?
Diagnosis of Acute Heptitis C infection:
[In short: ELISA, RIBA, PCR]
Actual answer:
1) Specimen: Blood
2) Serological test:
a. Antibody (IgM/IgG) detection by ELISA
b. RIBA (Recombinant immunobolt assay) confirmatory test
3) Nucleic acid base technique:
a. PCR (Polymerase chain reaction) Detects the presence of viral RNA in serum.
Ref: Lange
36. Why HDV is called defective virus?
HDV is called defective virus:
Because hepatitis D virus can not infect without the help of hepatitis-B virus.
37. Mode of transmission of HDV.
Mode of transmission of HDV:
1) Parenteral route
2) Sexual
3) Vertical
38. What do mean by superinfection and coinfection in case of hepatitis D virus (HDV)?
Coinfection:A patient can acquire hepatitis D virus infection at the same time as he/she is infected with
the hepatitis B virus. This is called co-infection.
Superinfection:A patient with hepatitis B can be infected with hepatitis D virus at any time after acute
hepatitis B virus infection. This is called super-infection.
Ref: http://www.natap.org/2002/Dec/120602_2.htm
39. Name neurotrophic viruses.
Neurotrophic viruses: [Mnemonic: pH-RH-MAN of Japan]
1) Polio
2) Herpes simplex-1, Herpes zoster
3) Rabies
4) HIV
5) Measles
6) Arbovirus
7) Nipah virus
8) Japanese B encephalitis
40. How rabies virus is transmitted to human?
Mode of transmission of rabies virus:
1) Animal bites
2) Licks
3) Aerosols of bat secretions containing rabies virus.
4) Person to person
a. Child biting to parents
b. Corneal and organ transplantation
[Ref: Lange 11th/259]
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Multiply in the lymphoid tissue in the oropharynx & small intestine (Peyers patches)
Go to the CNS (spinal cord & brain) via blood steam and also by retrograde spreading along nerve axons.
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2) Oral polio vaccine (OPV)/ Sabin vaccine or live attenuated polio vaccine
Advantages (Merit) of live vaccine/OPV:
1) Cheaper
2) Easy to administer
3) Produce local immunity. (Produce local gut immunity by provoking production of intestinal IgA)
4) Passive immunity by contamination with environment.
Disadvantages (Demerit) of live vaccine/OPV:
1) It may revert to virulence
2) It can also spread from vaccine to contacts.
3) Presence of other viruses may interfere with gut colonization.
4) Can not be given in pregnancy & immunosuppressed persons.
5) Multiple doses are necessary to establish immunity.
6) Must be kept refrigerated to prevent heat-inactivation.
Advantages (Merit) of Killed vaccine/IPV/Salk vaccine:
1) It does not revert to virulence.
2) It does not interfere with replication of virulent virus in gut.
3) Does not require refrigeration.
4) Does not cause disease in immunocompromised person.
Disadvantages (Demerit) of Killed vaccine/IPV/Salk vaccine:
1) Usually costly
2) Local pain during administration.
3) Duration of immunity is shorter.
49. What are the merits of OPV? What do you mean by viral interference during use of OPV?
Advantages (Merit) of live vaccine/OPV:
1) Cheaper
2) Easy to administer
3) Produce local immunity. (Produce local gut immunity by provoking production of intestinal IgA)
4) Passive immunity by contamination with environment.
Viral interference during use of OPV:
When OPV is given it interfere with non-polio viruses and can prevent otitis media.
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Organs:
Lymphoid organs
61. Mention the stages of HIV infection.
Stages of HIV infection:
The clinical picture of HIV infection can be divided into three stages
1) An early, acute stage: Fever, lethargy, sore throat and generalized lymphadenopathy.
Maculopapular rash on the trunk, arms and legs( but sparing the palms and soles), leucopenia. This
stage resolves spontaneously in about 2 weeks.
2) A middle, latent stage: A long latent period, measured in years, usually ensues. In untreated
patient, this stage last for 7-11 years.The patient is usually asymptomatic during this period.
3) A late, immunodeficiency stage: The late stage is the acquired immunodeficiency syndrome
(AIDS). This stage is characterized by marked reduction in the CD4 cells and occurrence of
opportunistic infection.
[Ref: Lange 11th/303]
62. What are the features of AIDS related complex (ARS). Mention its importance.
Features of AIDS related complex (ARS):
1) Unexplained diarrhea lasting longer than a month
2) Fatigue
3) Malaise
4) Loss of more than 10 percent body weight
5) Fever
6) Night sweats
Importance:
Some patients with AIDS related complex subsequently develop AIDS.
63. Define AIDS. Mention opportunistic infection in AIDS.
AIDS (Acquired Immuno Deficiency Syndrome):
It is a syndrome complex, which is caused by human immuno deficiency virus (HIV).
Opportunistic infection in AIDS:
A. Bacterial:
1) M. tuberculosis
2) M. avium intracellulare (MAI)
3) M. kansasii
4) Nocardia asteroids
5) Listeria monocytogenes
6) Salmonella
B. Viral:
1) Cytomegalovirus (CMV)
2) Herpes simplex virus
3) Herpes zoster
4) Hepatitis B virus (HBV)
C. Fungal:
1) Candida species
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2) Cryptococcus neoformans
3) Histoplasma species
D. Parasitic:
1) Pneumocystic carinii
2) Cryptosporidium species
3) Isospora belli
4) Strongyloides stercoralis
5) Sarcocystic species
Causes of opportunistic infection in AIDS:
HIV infects CD4 + T-cells. As a result there is loss of T-cell response to form cytotoxic T-cell and
proliferation and differentiation of B cell. So both the cell mediated and antibody mediated immunity is lost.
For this reason opportunistic pathogens cause severe disease.
64. How can you diagnose HIV infection in the laboratory?
Diagnosis of HIV infection:
1) Detection of antigen by ELISA
2) Confirmatory test by western blot.
[Specimen: Blood for serological test & culture]
65. What is dengue? Name vector & type of dengue virus.
Dengue ( breakbone fever):
Dengue is a mosquito-borne is an infectious tropical disease caused by the dengue virus.
Vector: Female Aedes aegypti mosquito
Types of dengue virus:
4 serological types:
1) DEN-1
2) DEN-2
3) DEN-3
4) DEN-4
66. Mention clinical types of dengue.
Clinical types of Dengue:
1) Primary Dengue (Classical dengue fever): When the patient is infected with any of four strain (DEN1, DEN-2, DEN-3, DEN-4)
2) Secondary Dengue (Dengue haemorrhagic fever): When the patient become infected with any of the
rest 3 strains again.
67. Tell pathogenesis of dengue shock syndrome.
Pathogenesis of dengue fever:
A. Classical dengue fever (First exposure of dengue virus):
Dengue infection by one of the four serotypes
Antibody is formed
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