Ch 20 Flashcards
(263 cards)
1
Q
What does “obligate intracellular parasite” mean in relation to viruses?
A
It means viruses must enter and use a host cell to reproduce. They cannot survive or multiply outside living cells.
2
Q
What type of genetic material do viruses contain?
A
Viruses contain either DNA or RNA, never both.
3
Q
What structures make up a virus?
A
A virus is made of a protein capsid and sometimes a lipid envelope.
4
Q
Why can’t viruses make their own proteins or energy?
A
They lack ribosomes and metabolic machinery, so they depend on the host cell for protein synthesis and energy.
5
Q
How do viruses enter the human body?
A
They must overcome barriers like the skin, mucous membranes, and the immune system.
6
Q
Why were viruses once called “filterable agents”?
A
Because they are so small, they could pass through filters that normally trap bacteria.
7
Q
Do all viruses have a lipid envelope?
A
No, some do, and some don’t. The envelope is usually taken from the host cell membrane.
8
Q
What are the main bases for classifying viruses?
A
• Structure (capsid shape, envelope)
• Genome type (DNA/RNA, single/double-stranded, segmented)
• Disease and transmission (e.g., hepatitis, arboviruses)
9
Q
What are the types of viral capsid structures?
A
• Icosahedral (20-sided)
• Helical (spiral shape)
• Naked capsid viruses are resistant to drying and survive in the GI tract
10
Q
What is a viral envelope and where does it come from?
A
A lipid bilayer taken from the host cell membrane, contains glycoproteins like HA/NA (seen in influenza).
11
Q
How can viral genomes differ?
A
They may be:
• DNA or RNA
• Single-stranded (ss) or double-stranded (ds)
• Segmented or non-segmented
12
Q
What are examples of classification based on disease and transmission?
A
• Hepatitis viruses (cause liver disease)
• Arboviruses (transmitted by insects like mosquitoes)
13
Q
What is the size range of viruses?
A
From 18 nm (e.g., Parvovirus) to 300 nm (e.g., Poxvirus)
14
Q
What is the capsid and its function?
A
The capsid is a protein shell that protects the viral genome.
In naked viruses, it helps them resist drying, acid, and bile.
15
Q
What is the viral envelope made of and what does it contain?
A
A lipid bilayer from the host cell, containing glycoproteins (e.g., HA/NA in influenza).
16
Q
What types of genomes can viruses have?
A
• DNA or RNA
• Linear or circular
• Positive-sense (+) or negative-sense (-) (for RNA viruses)
17
Q
What is a nucleocapsid?
A
It is the viral genome + capsid.
18
Q
What is VAP (Viral Attachment Protein) and its role?
A
A protein on the virus surface that binds to host cell receptors for entry.
Example: gp120 in HIV
19
Q
Capsid Viruses like ?
A
Poliovirus, Adenovirus
20
Q
Capsid Viruses Resistance to ?
A
Acid, bile, drying
21
Q
Capsid Viruses Transmintion by ?
A
Fecal-oral, stable
22
Q
Enveloped Viruses like ?
A
HIV, Influenza
23
Q
Enveloped Viruses Resistance to ?
A
Sensitive to detergents, heat
24
Q
Enveloped Viruses transmintion by ?
A
Fluid-borne, respiratory
25
What is the genome type of Group I viruses?
Double-stranded DNA (dsDNA)
26
How do Group I viruses replicate their genome?
Inside the nucleus using host DNA-dependent DNA polymerase (except Poxvirus which replicates in the cytoplasm)
27
Name two examples of Group I viruses.
Herpesvirus (enveloped), Adenovirus (naked), Poxvirus (enveloped, complex capsid)
28
Which Group I virus replicates in the cytoplasm and why?
Poxvirus, because it carries its own DNA polymerase.
29
What is the genome of Group II viruses?
Single-stranded DNA (ssDNA)
30
What must happen before Group II viruses can replicate?
Their ssDNA must be converted into dsDNA by host enzymes.
31
What is a common example of a Group II virus?
Parvovirus
32
Are Group II viruses enveloped or naked?
Naked (unenveloped)
33
What is the genome type of Group III viruses?
Double-stranded RNA (dsRNA)
34
Why can’t Group III viruses be directly translated by host ribosomes?
Because host ribosomes cannot use dsRNA, so the virus must bring its own RNA-dependent RNA polymerase.
35
Name an example of a Group III virus.
Reovirus
36
What is special about Reoviruses structurally?
They have a double capsid and a segmented genome.
37
What is the genome type of Group IV viruses?
Single-stranded RNA with positive polarity
38
Can Group IV RNA be directly translated into protein?
Yes, it acts like mRNA.
39
Name two Group IV viruses, one enveloped and one naked.
Coronavirus (enveloped), Picornavirus (naked)
40
What do many Group IV viruses cause?
GI and respiratory infections (e.g., polio, hepatitis A, COVID-19)
41
What is the genome of Group V viruses?
Single-stranded RNA with negative polarity
42
What must these viruses carry in their virion?
RNA-dependent RNA polymerase to transcribe (+) sense RNA
43
Name some examples of Group V viruses.
Influenza virus, Rabies virus, Filovirus (Ebola), Paramyxovirus
44
Are Group V viruses enveloped or naked?
All are enveloped
45
Which Group V viruses have segmented genomes?
Influenza virus (Orthomyxovirus), Bunyaviruses, Arenaviruses
46
What is the genome of Group VI viruses?
Positive-sense single-stranded RNA
47
What unique enzyme do Group VI viruses use?
Reverse transcriptase (RNA → DNA → host genome)
48
Name an example of a Group VI virus.
HIV (Retrovirus)
49
Where does replication occur in Group VI viruses?
In the nucleus, after integration into host DNA
50
What is the genome of Group VII viruses?
Partially double-stranded DNA
51
What happens after the virus enters the host cell?
The genome is completed to full dsDNA, transcribed to RNA, then reverse transcribed back to DNA.
52
Name a virus in Group VII.
Hepatitis B virus (Hepadnavirus)
53
Are Group VII viruses enveloped?
Yes
54
What is the first step of viral infection and what mediates it?
Attachment: Viral Attachment Protein (VAP) binds to a specific host receptor.
Example: HIV gp120 binds CD4 receptor.
55
How do viruses enter the host cell?
Penetration:
• Naked viruses: via endocytosis
• Enveloped viruses: via membrane fusion
56
What happens during uncoating?
Uncoating: The viral capsid is removed, and the genome is released into the cytoplasm or nucleus.
57
What occurs during macromolecular synthesis?
The virus uses host machinery to:
• Replicate its genome
• Produce viral mRNA and proteins
58
What happens during assembly?
Assembly: New virions are formed by combining:
• Newly made genome + capsid proteins
• ± Envelope if it’s an enveloped virus
59
How are new viruses released from the host cell?
Release:
• Naked viruses: by lysis (breaking the cell)
• Enveloped viruses: by budding from the cell membrane
60
Where do most DNA viruses replicate?
In the nucleus of the host cell
(Exception: Poxvirus replicates in the cytoplasm)
61
What enzyme do DNA viruses use for transcription?
Host RNA polymerase II
(Some large viruses like Herpesvirus have their own DNA polymerase)
62
Which DNA virus uses host enzymes completely?
HPV – uses host RNA polymerase and DNA polymerase
63
Where do most RNA viruses replicate?
In the cytoplasm
(Exceptions: Influenza and Retroviruses replicate in the nucleus
64
What enzyme is required for RNA virus replication?
RNA-dependent RNA polymerase (RdRp)
65
What’s special about +ssRNA viruses?
Their genome can act like mRNA and be directly translated
(Example: Poliovirus)
66
Why do –ssRNA viruses need RdRp in the virion?
Because –ssRNA cannot be directly translated, it must be converted to +ssRNA first
(Example: Influenza virus)
67
To which family does Adenovirus belong, and how many human serotypes are there?
Family: Adenoviridae
Human serotypes: 52 (classified into groups A–G)
68
What is the shape and size of Adenovirus?
Icosahedral symmetry, size 70–90 nm
69
Does Adenovirus have an envelope? What does this imply?
No envelope (naked virus) → resistant to drying, acids, and stable in GI/respiratory tracts
70
What is the genome type of Adenovirus?
Linear double-stranded DNA (dsDNA)
71
What structural proteins make up Adenovirus?
• 240 hexons (main capsid units)
• 12 pentons at the corners
• Fiber proteins for attachment to host cells
72
What is the role of fiber proteins in Adenovirus?
Help the virus attach to host cells; they also act as type-specific antigens
73
Is Adenovirus oncogenic in humans?
No, it is oncogenic in rodents, but not in humans
74
What major molecular biology discoveries came from studying Adenovirus?
Helped discover mRNA splicing and introns (non-coding regions in genes)
75
What receptors does Adenovirus use to attach to host cells?
Fiber protein binds:
• CAR (Coxsackie Adenovirus Receptor)
• or MHC-I
76
How does Adenovirus enter the host cell?
Via Clathrin-mediated endocytosis, triggered by penton–integrin interaction
77
What happens during uncoating of Adenovirus?
The endosome lyses, releasing the viral DNA into the nucleus
78
What do early genes (E1A, E1B) do?
•E1A: Pushes the host cell into cell cycle
•E1B: Helps virus evade apoptosis
79
What do late genes of Adenovirus encode?
They encode structural proteins needed for capsid assembly
80
Where does assembly of new Adenoviruses occur?
In the nucleus, where procapsids are formed and DNA is packaged
81
How are Adenoviruses released from the host cell?
By cell lysis
82
What type of cells does Adenovirus primarily target?
Mucosal epithelial cells in the respiratory, GI, and ocular tracts
83
What are VA RNAs and what do they do?
Virus-associated RNAs are short non-coding RNAs that block PKR, a host antiviral protein activated by interferon
84
Which viral proteins help Adenovirus evade the immune system?
•E3 and E1A proteins
•Inhibit apoptosis
•Suppress MHC-I presentation to avoid immune detection
85
What histopathologic feature is seen in Adenovirus infection?
Dense intranuclear inclusions without cytomegaly (unlike CMV)
86
What other histological changes are seen with Adenovirus infection?
• Mononuclear cell infiltration
• Epithelial cell necrosis
87
What are the main transmission routes of Adenovirus?
• Respiratory droplets
• Fecal-oral route
• Fomites (contaminated surfaces)
• Swimming pools
88
Which environments are high-risk for Adenovirus spread?
• Schools
• Military barracks
89
What makes Adenovirus environmentally resilient?
It resists:
•Drying
•Detergents
•Gastrointestinal secretions
90
What is asymptomatic shedding in Adenovirus?
Children can shed the virus in their feces for a long time, even without symptoms
91
Clinical symptoms of Adenovirus is ?
Febrile Pharyngitis
Pharyngoconjunctival Fever
Epidemic Keratoconjunctivitis
Gastroenteritis
Hemorrhagic Cystitis
Pneumonia (Immunocompromised)
92
Key Features of Febrile Pharyngitis is ?
Mimics strep throat in children.
93
Key Features of Pharyngoconjunctival Fever is ?
Conjunctivitis + sore throat.
94
Key Features of Epidemic Keratoconjunctivitis is ?
Occupational outbreaks (e.g.,
shipyards).
95
Key Features of Gastroenteritis is ?
Major cause of pediatric diarrhea.
96
Key Features of Hemorrhagic Cystitis is ?
Dysuria, hematuria in boys.
97
Key Features of Pneumonia (Immunocompromised) is ?
Life-threatening systemic spread.
98
What is the role of PCR in Adenovirus detection?
PCR detects the viral genome rapidly from samples like respiratory secretions or stool
99
What do ELISA and immunofluorescence detect in Adenovirus infection?
They detect viral antigens (proteins of the virus)
100
What cell lines are used to culture Adenovirus in the lab?
Human epithelial cells like HeLa or A549
101
What cytopathic effects are seen in Adenovirus culture?
•Cell rounding
•Dense intranuclear inclusions
102
What is the role of serology in Adenovirus diagnosis?
Detects neutralizing antibodies, especially against fiber proteins – useful in epidemiological studies
103
Is there an approved antiviral treatment for Adenovirus?
No approved antivirals – treatment is usually supportive care
104
What antivirals may be used off-label for immunocompromised patients?
Cidofovir or Ribavirin (used off-label)
105
How can Adenovirus transmission be prevented?
•Hand hygiene
•Chlorinated swimming pools
106
What is the Adenovirus vaccine used in the military?
Live oral vaccine for types 4 and 7
(Only for military personnel)
107
How are Adenoviruses used in gene therapy?
Modified viruses (E1/E3 deleted) are used as vectors to deliver genes for conditions like cystic fibrosis or ADA deficiency
108
What role does Adenovirus play in vaccine development?
Used as chimeric vectors in vaccines against:
• COVID-19 (SARS-CoV-2)
• HIV
• Ebola
109
What is ONYX-015 and how is it used?
A modified Adenovirus used in oncolytic therapy to target p53-deficient tumors
110
What is a major risk of using Adenovirus-based therapies?
May cause severe disease in immunocompromised patients
111
Key Features of heepisviruse
▪ Large, enveloped dsDNA viruses.
▪ Ubiquitous; cause lytic, latent, and recurrent infections.
112
What is the virus name of HHV-1?
Herpes Simplex Virus Type 1
113
What is the subfamily of HHV-1?
Alphaherpesvirinae
114
What is the primary target cell of HHV-1?
Mucoepithelial cells
115
What is the site of latency of HHV-1?
Neuron
116
What is the means of spread of HHV-1?
Close contact
117
What is the virus name of HHV-2?
Herpes Simplex Virus Type 2
118
What is the subfamily of HHV-2?
Alphaherpesvirinae
119
What is the primary target cell of HHV-2?
Mucoepithelial cells
120
What is the site of latency of HHV-2?
Neuron
121
What is the means of spread of HHV-2?
Close contact (sexually transmitted disease)
122
What is the virus name of HHV-3?
Varicella-Zoster Virus
123
What is the subfamily of HHV-3?
Alphaherpesvirinae
124
What is the primary target cell of HHV-3?
Mucoepithelial cells
125
What is the site of latency of HHV-3?
Neuron
126
What is the means of spread of HHV-3?
Respiratory and close contact
127
What is the virus name of HHV-4?
Epstein-Barr Virus
128
What is the subfamily of HHV-4?
Gammaherpesvirinae
129
What is the primary target cell of HHV-4?
B cells and epithelial cells
130
What is the site of latency of HHV-4?
B cell
131
What is the means of spread of HHV-4?
Saliva (kissing disease)
132
What is the virus name of HHV-8?
Kaposi’s Sarcoma-Related Virus
133
What is the subfamily of HHV-8?
Gammaherpesvirinae
134
What is the primary target cell of HHV-8?
Lymphocyte and other cells
135
What is the site of latency of HHV-8?
B cell
136
What is the means of spread of HHV-8?
Close contact (sexual), saliva?
137
What is the virus name of HHV-5?
Cytomegalovirus
138
What is the subfamily of HHV-5?
Betaherpesvirinae
139
What is the primary target cell of HHV-5?
Monocyte, lymphocyte, and epithelial cells
140
What is the site of latency of HHV-5?
Monocyte, lymphocyte
141
What is the means of spread of HHV-5?
Close contact, transfusions, tissue transplant, and congenital
142
What is the virus name of HHV-6?
Herpes Lymphotropic Virus
143
What is the subfamily of HHV-6?
Betaherpesvirinae
144
What is the primary target cell of HHV-6?
T cells
145
What is the site of latency of HHV-6?
T cells
146
What is the means of spread of HHV-6?
Respiratory and close contact
147
What is the virus name of HHV-7?
Human Herpesvirus 7
148
What is the subfamily of HHV-7?
Betaherpesvirinae
149
What is the primary target cell of HHV-7?
T cells
150
What is the site of latency of HHV-7?
T cells
151
What is the shape and composition of the herpesvirus capsid?
It is icosahedral in shape and composed of 162 capsomeres.
152
What is the function of the tegument in herpesvirus?
It contains viral proteins and enzymes that help in early infection, such as VP16.
153
What proteins are found in the herpesvirus envelope, and what is their function?
Glycoproteins gB and gD, which help in attachment to host cells and membrane fusion.
154
What type of genome does herpesvirus have?
Linear double-stranded DNA (dsDNA) with terminal repeats.
155
Why are terminal repeats in the herpesvirus genome important?
They enable the genome to circularize inside the host nucleus, aiding in replication.
156
What is the structure of herpesviruses in terms of capsid and genome?
They have a large, enveloped icosadeltahedral capsid and a double-stranded DNA (dsDNA) genome.
157
What important viral enzyme do herpesviruses encode?
DNA polymerase, which is a target for antiviral drugs.
158
Where does herpesvirus replication occur in the host cell?
In the nucleus.
159
How are herpesviruses released from infected cells?
By exocytosis, cell lysis, or direct cell-to-cell bridges.
160
What types of infections can herpesviruses cause?
Lytic, persistent, latent, or immortalizing infections.
161
How common are herpesviruses in the population?
They are ubiquitous (very widespread).
162
Which part of the immune system is essential for controlling herpesvirus infections?
Cell-mediated immunity (especially T cells).
163
How do herpesvirus infections differ between children and immunosuppressed individuals?
Usually mild in children but severe with high morbidity and mortality in immunosuppressed individuals.
164
What host receptor does HSV glycoprotein bind to during attachment?
Nectin-1.
165
What are the entry mechanisms of HSV into host cells?
Fusion with the membrane or endocytosis.
166
What happens after HSV enters the cell?
The capsid is delivered to the nucleus.
167
What is produced in the immediate early (α) phase of HSV gene expression?
Regulatory proteins like ICP4.
168
What is produced in the early (β) phase of HSV gene expression?
Enzymes like DNA polymerase and thymidine kinase.
169
What is produced in the late (γ) phase of HSV gene expression?
Structural proteins such as capsid proteins and glycoproteins
170
Where does HSV assemble and acquire its envelope?
It assembles in the nucleus, moves to the cytoplasm, and acquires its envelope from the Golgi.
171
How is HSV released from the host cell?
Via exocytosis or cell lysis.
172
What is genome persistence in neurons or lymphocytes?
Some viruses, like HSV and VZV, persist in neurons, while EBV and CMV persist in lymphocytes, staying dormant in these cells.
173
How does MHC I downregulation help viruses avoid immune detection?
HSV blocks antigen presentation by inhibiting MHC I expression, preventing the immune system from detecting infected cells.
174
What is the role of anti-apoptotic proteins in viral persistence?
EBV produces BHRF1 and CMV produces vICA to prevent infected cells from undergoing apoptosis (programmed cell death), allowing the virus to persist longer.
175
How do viruses mimic cytokines to avoid immune responses?
EBV and CMV produce proteins like BCRF1 and vIL-10 that mimic cytokines, tricking the immune system and helping the virus evade immune detection.
176
How do viruses avoid antibodies through cell-to-cell spread?
Some viruses, such as HSV, spread from one infected cell to another without releasing viral particles into the bloodstream, which helps them avoid detection by antibodies.
177
How do cell-mediated immunopathologic effects contribute to symptoms?
The symptoms of viral infections often arise from the immune system’s response to infected cells, rather than from the virus itself.
178
How is HSV transmitted?
HSV is transmitted through mucosal contact and vertically (from mother to neonate during childbirth).
179
What are the clinical syndromes caused by HSV?
Oral/Genital Herpes: Vesicular lesions that turn into ulcers.
• Encephalitis: Temporal lobe involvement, with 70% mortality (especially from HSV-1).
• Neonatal HSV: Disseminated disease with high mortality in newborns.
180
Where does HSV establish latency?
HSV-1 establishes latency in the trigeminal ganglia (face), and HSV-2 in the sacral ganglia (lower spine).
181
What is the rule of thumb regarding HSV-1 and HSV-2 infections?
HSV-1 generally causes infections above the waist (e.g., oral herpes), while HSV-2 usually affects below the waist (e.g., genital herpes).
182
Who is at risk for infection of the fingers by HSV?
Physicians, nurses, and dentists are at risk for herpetic whitlow (finger infection) caused by HSV-1 or HSV-2.
183
What is the primary infection caused by VZV?
Varicella (chickenpox), which presents as a diffuse, asynchronous vesicular rash.
184
Where does VZV remain latent after primary infection?
In the dorsal root ganglia.
185
What is herpes zoster and when does it typically occur?
Herpes zoster (shingles) is a reactivation of VZV causing a dermatomal rash and postherpetic neuralgia, usually in the fifth or sixth decade of life.
186
What are complications of VZV infection?
Pneumonia in adults and congenital defects if infection occurs during pregnancy.
187
What vaccines are available for VZV?
• Varivax: A live attenuated vaccine for chickenpox.
• Shingrix: A subunit vaccine for shingles.
188
How is Epstein-Barr Virus (EBV) transmitted?
Through saliva; it is commonly called the “kissing disease.”
189
What are the key features of infectious mononucleosis caused by EBV?
Fever, lymphadenopathy, and atypical lymphocytes.
190
What type of antibodies are produced during EBV infection and why?
Heterophile antibodies, due to B cell mitogenesis (activation and proliferation).
191
What cancers are associated with EBV?
Burkitt lymphoma and nasopharyngeal carcinoma.
192
What EBV-associated condition can occur in immunocompromised individuals?
Post-transplant lymphoproliferative disorder and hairy oral leukoplakia.
193
Where does EBV remain latent, and what protein does it express?
In memory B cells, with expression of EBNA-1 protein.
194
What are the modes of CMV transmission?
Congenital, sexual contact, blood transfusion, and organ transplantation.
195
What are the features of congenital CMV infection?
Hearing loss, microcephaly, “blueberry muffin” rash, and possible death.
196
How does CMV mononucleosis differ from EBV mononucleosis?
CMV mononucleosis is heterophile-negative, unlike EBV.
197
What diseases can CMV cause in immunocompromised individuals?
Retinitis, colitis, and pneumonitis.
198
How is CMV related to graft-versus-host reactions (GVHR)?
CMV may contribute to GVHR after bone marrow transplantation.
199
Where does CMV remain latent in the body?
In mononuclear cells.
200
What disease is caused by HHV-6 and HHV-7?
Roseola (Exanthem Subitum) – characterized by high fever followed by a rash.
201
What complications are associated with HHV-6/7?
Febrile seizures and DRESS syndrome.
202
What condition is caused by HHV-8?
Kaposi Sarcoma – cutaneous tumors, especially in AIDS patients.
203
What viral proteins are produced by HHV-8 that contribute to cancer?
Viral IL-6 and chemokine analogs (oncoproteins).
204
What is the natural host of Herpes B virus (Alphaherpesvirinae)?
Asian macaques (monkeys).
205
Is Herpes B virus zoonotic, and how dangerous is it to humans?
Yes, it’s zoonotic and rare but can cause severe or fatal infections in humans.
206
How can humans become infected with Herpes B virus?
Through monkey bites or scratches, contact with saliva/CNS tissue, or lab exposure.
207
Who is most at risk for Herpes B virus infection?
Veterinarians, laboratory workers, and primate handlers.
208
What are the early symptoms of Herpes B virus infection in humans?
Vesicular rash, pain, itching at the exposure site, and flu-like symptoms.
209
What severe complications can Herpes B virus cause?
Encephalomyelitis, ascending paralysis, respiratory failure, and neurological damage.
210
What is the fatality rate of Herpes B virus without treatment?
About 70%; survivors often have long-term neurological deficits.
211
What is the gold standard diagnostic test for HSV, CMV, and VZV?
PCR
212
What does a Tzanck smear show in HSV/VZV infection?
Syncytia and Cowdry A intranuclear inclusions.
213
What is a characteristic microscopic finding in CMV infection?
Owl’s eye inclusions (large intranuclear bodies).
214
What serologic test is used to diagnose EBV infection?
Heterophile antibody test.
215
Which antibody indicates an acute viral infection?
IgM
216
What cell type is used for culturing CMV?
Human fibroblasts.
217
What is the purpose of the rapid shell vial assay?
Faster detection of viruses like CMV after culturing.
218
Which nucleoside analogs are used for HSV and VZV?
Acyclovir and Valacyclovir.
219
What viral enzyme activates Acyclovir and Valacyclovir?
Thymidine kinase (TK).
220
Which drugs are used to treat CMV and HHV-6?
Ganciclovir and Valganciclovir.
221
What viral enzyme activates Ganciclovir?
UL97 kinase.
222
Which antiviral drugs inhibit DNA polymerase without needing thymidine kinase?
Foscarnet and Cidofovir.
223
How does resistance to herpes antivirals usually develop?
Through mutations in thymidine kinase or DNA polymerase genes.
224
What are the two vaccines available for VZV?
Varivax (live attenuated) and Shingrix (subunit).
225
Are there vaccines available for EBV, CMV, or HSV?
No, they are still under development.
226
What antiviral is used for HSV prophylaxis in immunocompromised patients?
Acyclovir.
227
What antiviral is used for CMV prophylaxis in immunocompromised patients?
Valganciclovir
228
How can neonatal HSV infection be prevented during childbirth?
Avoid vaginal delivery if the mother has active HSV lesions.
229
How is smallpox transmitted?
By aerosols, direct contact, and fomites → enters via inhalation.
230
Where does smallpox replicate first?
In the upper respiratory tract (URT), then spreads via viremia.
231
How is Molluscum contagiosum virus (MCV) transmitted?
Through direct skin contact (e.g. sexual) or contaminated objects (e.g. towels).
232
What are zoonotic poxvirus infections caused by?
Occupational or accidental exposure to infected animals.
233
What do poxvirus proteins do?
Promote cell growth, cause lysis, and help immune evasion.
234
Which type of immunity is essential to fight poxviruses?
Cell-mediated immunity (e.g., T-cells).
235
How do poxviruses evade the immune system?
They block interferons, complement, and antibodies.
236
How much of the poxvirus genome is for immune evasion?
More than 30%.
237
Which poxviruses are human-only?
Smallpox and Molluscum contagiosum virus (MCV).
238
What are the two main variants of smallpox?
Variola major (15–40% mortality) and Variola minor (1% mortality).
239
What are the key symptoms of smallpox?
Fever, headache, and rash—all appear simultaneously.
240
Where does the smallpox rash start?
In the mouth, then spreads to the rest of the body.
241
What is variolation?
An old method using virulent material from a smallpox patient to induce immunity.
242
What are Guarnieri bodies?
Intracytoplasmic inclusion bodies found in smallpox-infected cells.
243
How is smallpox mainly diagnosed?
Clinically, supported by the presence of pocks and Guarnieri bodies.
244
What tool is used to give the smallpox vaccine?
A bifurcated needle.
245
What is encephalitis in the context of smallpox vaccination?
A rare but serious complication involving brain inflammation.
246
What is vaccinia necrosum?
Severe tissue destruction at the vaccination site, usually in immunocompromised people.
247
Can the vaccinia virus spread to others from the vaccinated person?
Yes, by direct contact with the vaccination site.
248
How is accidental vaccinia infection in contacts treated?
With immune globulin.
249
How common is molluscum contagiosum?
It affects 3–20% of the population.
250
What do molluscum nodules look like?
Pearl-like, umbilicated (central dimple), 2–10 mm in size, usually fewer than 20.
251
Where do molluscum lesions commonly appear?
On the trunk, genitals, and extremities.
252
Who is commonly affected by molluscum contagiosum?
Children, sexually active individuals, and immunocompromised patients.
253
How is molluscum contagiosum diagnosed microscopically?
By finding cytoplasmic inclusions called molluscum bodies.
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Where does the virus replicate?
In keratinocytes (skin cells only).
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How does molluscum contagiosum affect infected cells?
Stimulates growth, prevents apoptosis, and releases virus when cells mature.
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Is molluscum contagiosum cytolytic?
No, it is non-cytolytic—does not kill the cell directly.
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Which virus does molluscum contagiosum’s lifecycle resemble?
Human papillomavirus (HPV).
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Which hybrid poxviruses are used in gene therapy?
Vaccinia and Canarypox.
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What are three main uses of hybrid poxviruses in medicine?
Expression of foreign genes, oncolytic therapy, and gene replacement.
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What is meant by “expression of foreign genes”?
Using the virus to produce proteins from other organisms to stimulate the immune system.
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What is oncolytic therapy?
Using modified viruses to selectively infect and destroy cancer cells.
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What is gene replacement in this context?
Delivering healthy genes to cells to replace defective ones.
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What is a real-life example of using poxviruses in vaccines?
Rabies bait vaccines for wild animals using modified vaccinia virus.
