Ch 25 Flashcards
(147 cards)
1
Q
What virus family does Rubella belong to?
A
Matonaviruses – non-cytolytic, respiratory transmission.
2
Q
What type of genome does Rubella virus have?
A
Single-stranded positive-sense RNA (ss +ve RNA).
3
Q
What surface protein does the Rubella virus carry?
A
Hemagglutinin.
4
Q
Where does Rubella virus replicate in the host cell?
A
In the cytoplasm.
5
Q
What disease is caused by Rubella virus in children?
A
Mild exanthem known as “3-day measles” or “German Measles”.
6
Q
What can Rubella infection cause during pregnancy?
A
Severe congenital defects (e.g., congenital rubella syndrome - CRS).
7
Q
How does Rubella virus enter the body?
A
Through the respiratory tract.
8
Q
After entry, where does Rubella virus first replicate?
A
In local lymph nodes, causing lymphadenopathy.
9
Q
What happens during viremia in Rubella infection?
A
The virus spreads systemically, causing rash and joint pain (arthralgia).
10
Q
How does Rubella affect fetal development?
A
It is non-cytolytic but disrupts fetal cell growth/mitosis — teratogenic.
11
Q
When is Rubella contagious?
A
From 2 weeks before the rash (prodrome) until 2 weeks after the rash.
12
Q
When do antibodies appear in Rubella infection?
A
With the appearance of the rash.
13
Q
What do Rubella antibodies do?
A
Prevent viremia and provide lifelong immunity (1 serotype only).
14
Q
What immune component clears the Rubella infection?
A
Cell-mediated immunity.
15
Q
What causes rash and joint pain in Rubella?
A
Immune complexes (antibody + virus).
16
Q
How is the fetus protected from Rubella?
A
Maternal antibodies block transmission during pregnancy.
17
Q
What type of rash is seen in pediatric rubella?
A
3-day maculopapular rash.
18
Q
What lymphatic symptom is common in children with rubella?
A
Lymphadenopathy.
19
Q
How severe is the fever in pediatric rubella?
A
Mild fever.
20
Q
What is the incubation period for rubella?
A
14–21 days.
21
Q
What percentage of pediatric primary infections are subclinical?
A
20–50%.
22
Q
What joint-related symptoms occur in adult rubella?
A
Arthralgia or arthritis.
23
Q
What rare blood-related complication can occur in adults?
A
Rare thrombocytopenia.
24
Q
What neurological complication may occur post-infection in adults?
A
Post-infectious encephalopathy.
25
What eye and ear defects can CRS cause?
Cataracts and deafness.
26
What heart-related defect can CRS cause?
Cardiac defects.
27
What brain-related defect is common in CRS?
Microcephaly.
28
What is the mortality risk for CRS?
High mortality (in utero or first year of life).
29
When is CRS most likely to occur during pregnancy?
During the first 20 weeks of pregnancy.
30
How is rubella transmitted?
Through respiratory droplets.
31
How long can the rubella virus persist in the eye lens of a CRS infant?
3–4 years.
32
How long can an infant with CRS shed the virus?
Up to 1 year after birth.
33
What is the only host for rubella virus?
Humans.
34
Who commonly gets rubella infection?
Children.
35
What test detects viral RNA in rubella diagnosis?
RT-PCR (from urine or respiratory samples).
36
Which test confirms acute rubella infection?
IgM ELISA.
37
Is there any antiviral treatment for rubella?
No, treatment is supportive only.
38
What vaccine strain is used for rubella?
RA27/3 strain (live attenuated).
39
In which vaccine is rubella included?
MMR vaccine (Measles, Mumps, Rubella).
40
Can pregnant women receive the rubella vaccine?
No, it is contraindicated in pregnancy.
41
What is the shape and size of Arenaviruses?
Pleomorphic enveloped viruses
42
What gives Arenaviruses their characteristic sandy appearance?
The presence of host ribosomes inside the virion.
43
How many RNA segments do Arenaviruses have, and what are they called?
Two single-stranded RNA segments: S and L.
44
What does the S segment of Arenaviruses encode?
It encodes the N protein and glycoproteins; it is ambisense and about 3400 nucleotides long.
45
What does the L segment of Arenaviruses encode?
It encodes RNA polymerase; it is negative-sense and about 7200 nucleotides long.
46
Where does replication of Arenaviruses occur?
In the cytoplasm, with budding from the plasma membrane.
47
Why do Arenaviruses cause persistent infections?
Due to inefficient transcription of the glycoprotein gene.
48
What are the main Arenaviruses that infect humans?
LCM virus, Lassa virus, Junin virus, Machupo virus.
49
What types of infections are Arenaviruses associated with?
Persistent infections and hemorrhagic fevers.
50
Which cells do Arenaviruses primarily infect?
Macrophages.
51
What immune response is triggered by Arenavirus infection of macrophages?
Production of cytokines and interferons.
52
How do Arenaviruses contribute to tissue damage?
By promoting vascular and cellular damage
53
What role does the immune system play in worsening Arenavirus infections?
T-cell–mediated immunopathology exacerbates tissue injury.
54
What is the typical incubation period for Arenavirus infections?
10–14 days.
55
What is the animal reservoir for Arenaviruses?
Specific rodent species.
56
What is the role of rodents in Arenavirus epidemiology?
They are chronic, asymptomatic carriers of the virus.
57
How do humans typically get infected with Arenaviruses?
Through inhalation of aerosols or contact with contaminated food and fomites.
58
What rodents are commonly associated with LCM virus?
House mice (Mus musculus) and hamsters.
59
How is Lassa virus transmitted between humans?
Via body fluids.
60
What are the common symptoms of LCM infection?
Flu-like febrile illness with muscle pain (myalgia).
61
What percentage of LCM cases progress to CNS infection?
Less than 10%.
62
When does meningitis typically appear in LCM infection?
Around 10 days after initial symptoms.
63
What is the typical outcome of LCM infection?
Recovery is usually complete.
64
What is a key histopathological finding in LCM-related CNS infection?
Perivascular mononuclear infiltrates in the brain.
65
What are the general symptoms of Arenavirus hemorrhagic fevers?
Fever, coagulopathy, petechiae.
66
What are the internal organ effects of hemorrhagic Arenavirus infections?
Visceral hemorrhage and necrosis of liver and spleen.
67
Are CNS lesions or vasculitis typical in Arenavirus hemorrhagic fevers?
No, they are not typically present.
68
What additional symptoms may occur in Lassa fever?
Pharyngitis, diarrhea, and vomiting.
69
What is the mortality rate of Lassa fever?
Up to 50%.
70
How does the mortality of Junin and Machupo virus infections compare to Lassa?
Their mortality rates are lower than Lassa fever.
71
What are the preferred methods for diagnosing Arenavirus infections?
Serology and RT-PCR.
72
What biosafety level is required for working with LCM virus?
Biosafety Level 3 (BSL-3).
73
What biosafety level is required for Lassa and other hemorrhagic viruses?
Biosafety Level 4 (BSL-4).
74
What antiviral drug has limited efficacy against Arenavirus infections?
Ribavirin, especially for Lassa fever.
75
What is the mainstay of treatment for Arenavirus infections?
Supportive care.
76
What family were Filoviruses previously classified under?
Rhabdoviridae
77
What are the main viruses included in the Filoviridae family?
Marburg virus and Ebola virus.
78
What is the structure of Filoviruses?
Filamentous, enveloped, negative-sense RNA viruses.
79
What type of disease do Filoviruses cause?
Severe or fatal hemorrhagic fevers.
80
What is the typical shape and size of Filoviruses?
Filamentous; 80 nm in diameter and 800–1400 nm in length.
81
What does the viral envelope of Filoviruses contain?
Glycoprotein (GP) that is cleaved into two forms, including a secreted shorter form.
82
What is the structure of the nucleocapsid in Filoviruses?
Helical.
83
Which receptors are used by Filoviruses to enter host cells?
NPC1 and TIM-1 (also used by Hepatitis A virus).
84
Where does replication of Filoviruses occur?
In the cytoplasm of host cells.
85
What is the mode of entry of Filoviruses into host cells?
Endocytosis.
86
What host mechanisms do Filoviruses use during replication?
Host machinery is used to replicate viral RNA and synthesize proteins.
87
Which cells show high levels of Filovirus replication?
Endothelial cells, monocytes, macrophages, and dendritic cells.
88
What immune reaction is triggered by Filovirus infection?
Cytokine storm, leading to sepsis-like symptoms.
89
Which organs are primarily affected by tissue necrosis in Filovirus infections?
Liver, spleen, lymph nodes, and lungs.
90
What causes vascular damage in Filovirus infections?
Cytolysis and loss of adhesion proteins in endothelial cells.
91
What role do glycoprotein gene mutations play in Filovirus infections?
They affect the severity of the hemorrhagic symptoms.
92
What are the effects of widespread hemorrhage in Filovirus infections?
Edema, hypovolemic shock, and disseminated intravascular coagulation (DIC).
93
How do Filoviruses evade the immune system?
By avoiding both innate (interferon response) and adaptive immune responses.
94
How is Filovirus transmitted between humans?
Through contact with blood and body secretions.
95
What are the initial symptoms of Filovirus infection?
Flu-like symptoms: fever, headache, and muscle pain (myalgia).
96
What symptoms appear as the infection progresses?
Nausea, vomiting, diarrhea, and rash.
97
What severe symptoms may develop in advanced Filovirus infections?
Gastrointestinal hemorrhage and multi-organ failure.
98
What is the fatality rate in clinically apparent Filovirus infections?
Up to 90%.
99
What is the mainstay of treatment for Filovirus infections?
Supportive care.
100
What is the name of the approved Ebola vaccine?
rVSV-ZEBOV.
101
What is the rVSV-ZEBOV vaccine composed of?
A recombinant vesicular stomatitis virus (VSV) expressing Ebola virus glycoprotein (GP).
102
What virus family and genus does Hepatitis C Virus (HCV) belong to?
Flaviviridae family, Hepacivirus genus.
103
What are the size and structure of HCV?
30–60 nm, enveloped virus with positive-sense RNA (~9100 nucleotides).
104
How many proteins does HCV encode, and what are some examples?
Encodes 10 proteins, including envelope proteins E1 and E2.
105
What feature of HCV’s RNA polymerase contributes to its antigenic variability?
The RNA polymerase is error-prone, leading to high mutation rates.
106
What type of hepatitis is HCV a major cause of?
Posttransfusion hepatitis.
107
What is the primary mode of HCV transmission?
Bloodborne transmission.
108
Is sexual transmission of HCV common?
It is possible but much less common than blood transmission.
109
Who are considered high-risk groups for HCV infection?
IV drug users, individuals co-infected with HIV, and babies born to HCV-positive mothers.
110
What host cell receptors are involved in HCV entry?
CD81, SRB1, claudin-1, occludin, and lipoprotein receptor.
111
Which human cells does HCV bind to?
Hepatocytes and B lymphocytes.
112
Which HCV protein inhibits apoptosis and IFN-α pathways?
NS5A (along with other viral proteins).
113
How does HCV promote persistent infection?
It is cell-associated and prevents host cell death.
114
How does HCV evade the immune system?
By evading the IFN response and mutating to escape immunity.
115
What happens to CD8+ T cells in chronic HCV infection?
They become exhausted, contributing to chronic infection.
116
What are the long-term consequences of HCV infection on the liver?
Chronic inflammation, fibrosis, and potential development of hepatocellular carcinoma (HCC).
117
What has significantly reduced HCV transmission rates?
Screening of blood products.
118
What percentage of HCV infections present as acute hepatitis?
About 15%, usually resolving with full recovery.
119
What percentage of HCV infections become chronic?
Approximately 70%.
120
What is the risk of rapid progression to cirrhosis in HCV patients?
Around 15%.
121
What are common symptoms of chronic HCV infection?
Chronic fatigue and mild signs of hepatitis.
122
What are potential long-term complications of chronic HCV infection?
Cirrhosis and hepatocellular carcinoma (HCC).
123
What does ELISA detect in HCV diagnosis?
Anti-HCV antibodies.
124
When does seroconversion typically occur in HCV infection?
Between 7–31 weeks after infection.
125
What are the gold standard tests for detecting HCV RNA?
RT-PCR and branched-DNA assays.
126
What are the three main classes of Direct Acting Antivirals (DAAs)?
1. Protease inhibitors
2. Nucleoside analog polymerase inhibitors
3. NS5A inhibitors
127
What older treatment was used for HCV before DAAs?
Interferon-alpha (IFN-α) combined with ribavirin.
128
What prevention methods help reduce HCV spread?
• Screening blood/organs
• Avoiding needle sharing
• Practicing safe sex
129
Why should HCV patients avoid alcohol?
It worsens liver damage.
130
What virus family does Hepatitis G Virus (HGV/GBV-C) belong to?
Flavivirus family, similar to HCV.
131
How is HGV primarily transmitted?
Through blood.
132
What condition is HGV associated with?
Chronic hepatitis.
133
What methods are used to detect HGV?
RT-PCR and other RNA-based detection methods.
134
What family does Hepatitis E Virus (HEV) belong to, and what are its features?
Hepeviridae family; it is a non-enveloped, positive-sense RNA virus.
135
What is the primary mode of transmission for HEV?
Fecal-oral route, especially via contaminated water.
136
What type of disease does HEV cause?
Only acute hepatitis, similar to Hepatitis A Virus (HAV).
137
How do HEV symptoms differ from HAV symptoms?
HEV symptoms may appear later than those of HAV.
138
What is the mortality rate of HEV in the general population?
About 1–2%.
139
What is the mortality rate of HEV in pregnant women?
Up to 20%.
140
What is the first step in HCV diagnosis?
Testing for anti-HCV antibodies.
141
What does a positive anti-HCV result indicate?
Requires confirmation with Core Ag or RNA testing.
142
What does a positive Core Ag or RNA result indicate after anti-HCV positivity?
Active HCV infection.
143
What does a repeatedly negative Core Ag or RNA result indicate after anti-HCV positivity?
Resolved HCV infection.
144
What are two possible explanations for a negative anti-HCV but positive Core Ag or RNA result in high-risk patients?
1. Window period before seroconversion (acute infection)
2. Immunocompromised state (current active infection)
145
What is the next step if anti-HCV is negative in a high-risk patient?
Test for Core Ag or RNA.
146
What does a negative Core Ag or RNA result indicate in high-risk patients?
HCV negative, but retesting in 6 months is recommended.
147
What does a negative anti-HCV result mean in a low-risk patient?
Likely HCV negative, no further testing needed.
