Virology Flashcards
1
Q
Regeneron
A
cocktail of MONOCLONAL antibodies directed against spike proteins
antibodies injected & useful in early infection
2
Q
Paxlovid (Pfizer)
A
oral antiviral (prescription) that inhibits viral replication
needs to be taken early on
3
Q
Molnupiravir (Merck)
A
oral antiviral (prescription) that causes mutations in viral RNA
4
Q
RT-PCR
A
detects RNA genome of virus that uses reverse transcriptase. it is for current infections and is high specific (+ and -)
5
Q
Antigen test
A
detects viral proteins using ELISA technology (only +)
6
Q
The best preventative for unimmunized against SARD COVID-19 is
A
social distancing & masks
7
Q
Viruses are considered nonliving because
A
they aren’t self replicating and rely on hosts for replication
8
Q
Since most viruses are tiny little *****, which microscope is needed to see them?
A
Electron Microscope
9
Q
A virion (virus particle) consists of nucleus acid surrounded by a protein coat. what is the name of this coat?
A
capsid
10
Q
what are the two types of virion?
A
Naked: w/o envelope (naked &afraid bc they lack that fatty wall😔)
Enveloped: surrounded by lipid membrane containing matrix proteins
11
Q
Viral genome contains only single type of nucleic acid, either DNA or RNA. which of these is unstable and causes faster changes?
A
RNA
12
Q
What is a viruses biggest weakness when it comes to replication?
A
it is an obligate intracellular parasite
13
Q
Every virus contains information to encode proteins for:
a) viral protein coat
b) replication of viral nucleic acid
c) movement in & out of host cells
d) needed enzymes NOT present in infected cell
e) all of the above
A
e) all of the above
14
Q
Viruses live in these two phases
A
Extracellular phase (Metabolically inert)
outside of living cells, viruses can’t thrive
Intracellular phase (Metabolically active)
15
Q
Lytic cycle
A
phage lyses infected cell and takes over cellular metabolic processes
*lyse means breakdown of a cell by causing damaging to plasma membrane (cell wall)
16
Q
Non-Lytic cycle
A
phage extrudes out of infected cell and only partially take over cellular metabolic pathways
Ex. filamentous phages
17
Q
T/F Bacteriophage integrates into genome
A
T
18
Q
T/F In a lytic cycle, a phage goes into the host cell as one, lyses, then leaves the cell as many
A
T
19
Q
Lysogenic state
A
phage integrate into host genome or DNA replicates as a plasmid (temperate phages)
20
Q
Lysogenic conversion
A
phage DNA codes for proteins that modify the properties of the bacterium
21
Q
Six stages of lytic phage replication by dsDNA phages:
A
1) attachment
2) penetration (stab & inject)
3) transcription
4) replication
5) assembly /maturation
6) release
22
Q
T/F Following attachment, phage DNA is injected into the bacterial cell, leaving the phage coat outside
A
T
23
Q
During transcription/replication in the lytic cycle, the virus will…
A
-inhibit activity of host DNA
-produce enzymes to destroy host DNA
- have Viral DNA take over & produce proteins
- early viral proteins are synth. and assoc. w/ replication of viral nucleic acid
-late viral proteins are synth. and assoc. w/ other viral structures
24
Q
T/F As viruses leave the host cell, the envelope is picked up only for eukaryotic viruses
A
T
25
T/F A lysogenic state integrates
T
26
prophage
integrated phage DNA
27
Lysogenic cell
bacterial cell carrying prophage
28
Steps of Lysogenic cycle
1) attachment
2) penetration
3) incorporation
29
In the lysogenic state, the host chromosome allows the phage to integrate bc...
sequences in the phage & bacterial chromosome are identical
30
T/F Phage repressor protein binds phage operator to inhibit expression of excision and lysis genes
T
31
Examples of phages carrying bacterial toxins
-cholera toxin
-diphtheria toxin
*shiga toxin*
32
ssDNA Filamentous phages are assembled & extruded from the cell wall w/o losing the cell. due to this, their DNA replication and synthesis of phage proteins cause bacterial growth to occur my slowly. In E.coli, the phages attach to the tip of the sex pilus but only infect which strain?
F+
F+
33
Transduction
DNA is transferred from one bacterial cell(donor) to another (recipient)
34
what is a way that antibiotic resistance gets moved around?
generalized transduction
35
Sites can be altered by two mechanisms:
mutation & lysogenized bacteria
36
Bacteria have two genes encoding for restriction-modification system:
endonuclease (cuts small segements of DNA that recognize viral DNA)
methylated bases
37
Phage therapy
use bacteriophage as antibacterial to treat patients
38
phage lysine as antimicrobials
use phage enzyme to treat infections as opposed to whole phage
39
CRISPR (clustered regularly interspaced short palindromic repeats)
phage spacer DNA inserted into CRISPR, provides record of infection
-Transcribed, cut
-small RNAs bind to CAS (CRISPR associated sequences)
-binding of spacer RNA to phage targets phage for destruction
40
Taxonomic criteria based on
-genomic structure
-virus particle structure
-presence or absence of envelope
41
enteric virus
transmitted via fecal-oral route
often cause gastroenteritis
42
respiratory virus
Usually inhaled via infected respiratory droplets
Generally remain localized in respiratory tract
43
zoonotic virus
transmitted from animal to human via animal vector
rabies
44
sexually transmitted virus
can cause lesions on genitalia or cause systemic infections
HIV
45
Types of infections
Acute & persistent
46
acute infection
-short in duration
- host may develop long lasting immunity
-produce large # of viruses during replication
-tissue damage & infection of new cells
47
persistent infections
-viruses continuously present in host
-can be divided into 3 categories:
-Latent(periods of no virus then reactivation...HSV-1)
-Chronic(virus always present at high levels...HBV)
-Slow(virus increases over time, disease late...HIV)
48
latent infection
-provides integrated into host chromosome or replicated separately
-cannot be eliminated
-can later be reactivated
ex. herpes & chicken pox—> adult=shingles
49
Reproductive cycle of animal virus
1) attachment
2) entry into susceptible cell
3) targeting site of reproduction
4)uncoating of virion
-exposes nucleic acid
5) replication of nucleic acid & protein
6) maturation
7) cell lysis
8) speeding w/in host
9) shedding outside host
10) transmission to next host
50
enveloped virion and the plasma membrane of the host may
fuse or the virion may be taken into cell by endocytosis
51
naked virion enter by endocytosis but do not
fuse with the vesicle membrane
52
Stages of the viral growth cycle
-Attachment and penetration by parental virion
-Uncoating of the viral genome
-Early viral mRNA and protein synthesis
-Viral genome replication
-Late mRNA and protein synthesis
-Progeny virion assembly
-Virion release from the cell
53
viral mRNAs have
-A methylated GTP cap
-A poly A tail
-mRNA generated by splicing
54
some viruses make more than one type of RNA from one piece of DNA by
shifting of the reading frame
55
How do some DNA viruses exercise temporal control of transcription
depressor protein prevents transcription of some genes until later
56
diff processes used to generate the monistic mRNAs that code for single protein from polycistronic viral genome
-individual mRNAs transcribed by starting at many specific initiation points (herpesviruses, adenoviruses, tumor viruses)
-genome may be segmented into multiple pieces, each coding for single mRNA (reoviruses & influenza)
-entire genome is translated into one long polypeptide which is then cleaved into specific proteins by protease (poliovirus)
57
enveloped virgins acquire the envelope though the
golgi apparatus, nuclear of cytoplasmic membrane
58
T/F most cells die due to take over of host cell machinery by virus
T
59
Retroviruses (HIV)
-contain 2 copies of ssRNA &RT
-ssRNA converted to dsDNA by RT
-dsDNA integrated into to host genome as provirus
-infection may be latent or productive
-viral DNA is transcribed by host RNA polymerase into polycistronic mRNA
-mRNA is translated into long polyprotein
-polyprotein is cleaved by viral encoded protease
60
genetic reassortment
two viruses infecting the same cell
61
T/F Reassortment is responsible for antigenic shift in influenza virus
T
lead to change in viral surface hemagglutinin expression & inability of antibodies to recognize new influenza strain
loss of herd immunity leading to past & future pandemics
62
T/F viruses can alter properties via point mutations
T
63
Tumor virus interacts with/host cells in one of two ways
-virus can go thru productive cycle and lyse (lytic cycle does NOT lead to tumor formation)
-virus can transform cell w/o killing it (CAN lead to tumor formation)
64
cancers caused by viruses can result from
-Encoding proteins that promote uncontrolled cell growth (stimulation of signal transduction pathways that regulate cell growth)
-Integration of viral oncogenes (causes malignant transformation of normal cells into cancer cells) into host DNA (HTLV-1)
-Activation of host cell proto-oncogenes (involved in host cell growth regulation) by integrating into a key regulatory area
65
plaque assay
Determines the number of viruses in solution. A known volume of solution is added to metabolizing cells, and the infection lyses cells and leads to a clear zone or plaque surrounded by uninfected cells. Each plaque represents one virion.
66
Hemagglutinin
causes clumping of red blood cells
spike protein attaches to RBC
67
viral infected plants may be recognized via outward signs
-pigment loss
-marks on leaves &fruit
-tumors
-stunted growth
*plants generally DONT recover from infections
68
Spread of plant viruses
-Viruses infect plants through wound in plant cell wall
-Plant viruses do not attach to specific cell receptors
-Once started, infection spreads from cell to cell through plasmodesmata
-Many viruses resistant to inactivation
-Viruses can be transmitted through soil contaminated by prior growth
-Viruses spread through grafting healthy plants to infected plants
-Viruses can spread via parasitic vine called fodder
-vine establishes simultaneous connection btwn 2 plants
-serves as conduit of transfer
69
Prions
-Proteinaceous infectious particles
-linked to fatal human diseases
-afflictions cause brain degeneration
-brain tissue develops sponge like holes
-sides termed transmissible spongiform encephalopathies
*symptoms may not appear for years after infection
70
T/F normal proteins &prions are resistant to UV light and nucleases
T
71
T/F prions are inactivated by chemicals that denature proteins
T
72
T/F antiviral chemicals interfere with viral replication
T
73
In regards to our current options, antiviral medications are not effective against latent infections.
T
74
A successful anti-viral will:
-Interfere with a virus-specific function
-Interfere w/a cellular function ao that the virus cannot replicate
-Toxicity may be acceptable if there is no other alternative
75
Potential anti-viral targets include:
-Attachment
-Viral uncoating
-Transcription of viral genome
-Translation to proteins
-Post-translational modification of proteins
-Assembly
76
Protease inhibitors are used to treat....
AIDS patients
77
Enfuvirtide
binds to an HIV protein that promotes fusion of viral envelope with cell membrane
**Prevent viral entry**
78
Maraviroc
blocks HIV co-receptor CCR5
**Prevent viral entry**
79
amantadine and rimantidine interfere with...
viral uncoating; nucleic acid must separate from protein coat
*block influenza A viruses*
80
Anti-viral drugs that block viral nucleic acid synthesis are selective because
-virus can use its own enzyme to activate drug
-viral polymerases are much more sensitive to the drug than the corresponding host enzymes
81
T/F Most nucleic acid synthesis inhibiting drugs are nucleoside analogs with an altered sugar, base or both
T
82
Nucleoside analogs
-similar in structure to nucleoside
-analogs phosphorylated & become nucleotide analogs
-Incorporation of analog results in chain termination /defective strand
83
Examples of nucleoside analogs
-Acyclovir, Valaciclovir, Penciclovir, Famciclovir, Ganciclovir
-Ribavarin
-AZT
-DDI
-3TC
84
Acyclovir
-herpes simplex virus thymidine kinase
-blocks DNA synthesis (chain terminator)
-effective against:
-HSV-1 (fever blisters)
-HSV-2 (genital herpes)
-HS keratitis (HSV-1)
-Varicella-Zoster Virus (chicken pox, shingles)
85
Ganciclovir
-active against CMV (cytomegalovirus)...in children
-used predominantly in AIDS patients
86
Nucleoside inhibitors of reverse transcriptase
-AZT
-DDI
-DDC
-chain terminators
-typically used in combos
87
Molnupiravir (Merck)
(Lageviro)
-nucleoside analog to promote high level of mutation in viral RNA (NOT chain terminator)
88
Non-Nucleoside Polymerase Inhibitors
-inhibit viral polymerases by binding to site other than nucleotide binding site
-Foscarnet used to treat ganciclovir-resistant CMV & acyclovir resistant HSV
89
Non-nucleoside Reverse Transcriptase Inhibitors (NNRTIs) inhibit reverse transcriptase by binding to the site other than nucleotide-binding site
-often used w/nucleotide analogs to treat HIV infections
-Include nevirapine, delaviridine, efavirenz
90
Prevent Genome Integration
-inhibit HIV-encoded enzyme integrase; prevent virus from inserting DNA copy of genome into host cell
-Raltegravir
91
Prevent Assembly & Release of viral particles
-During replication of HIV, several proteins are translated as a polyprotein that must be cleaved
-Includes indinavir, ritonavir, saquinavir, nelfinavir
92
Neuraminidase Inhibitors
-enzyme encoded by influenza viruses, needed for release
**most commonly used**
93
Protease inhibitors
inhibit HIV encoded enzyme protease
-Ex. indinavir & ritonavir
94
Highly Active Anti-Retroviral Therapies (HAART)
-combo therapy consisting of AZT, lamivudine (3TC), and protease inhibitor
95
Antivirals against COVID19
Paxlovid (Pfizer) (nirmatrelvir)
-SARSCOV2 Protease inhibitor
-inhibits viral replication
-for mild-moderate COVID-19
96
Neuraminidase (sialidase) inhibitors
-inhibit neuraminidase enzyme of influenza
-enzyme essential for release of virus
-Ex. zanamivir(inhalation) & oseltamivir(Tamiflu)(orally)
**Effective against influenza A & B**
97
HIV Disease belongs to
lentivirus subgroup of retrovirus family (ssRNA virus)
98
HIV symptoms
-Appear after incubation period of 6 days-6 weeks
-"Flu-like" symptoms (fever, headache, sore throat, muscle aches), enlarged lymph nodes & generalized rash
-Symptoms constitute acute retroviral syndrome (ARS)
-Acute illness followed by asymptomatic period
-AIDS-related complex (ARC)
-fever, weight loss, fatigue, & diarrhea
-tumors or opportunistic infections
99
HIV Pathogenesis
-HIV attacks variety of cell types
-After entry, DNA copies of RNA genome produced using reverse transcriptase viral enzyme
-In activated cells virus leaves cell genome & kills cell
-Macrophages have CD4 receptors
-Eventually immune system becomes too impaired to respond
100
HIV gene products & function
-Gp160, encoded by the env gene, is cleaved after translation by host enzymes to form gp120 & gp41
-Group-specific antigen gene (gag)
(made as polypeptide then cleaved by protease)
-Pol gene
101
HIV pathogenesis
(destruction of immune system helper T cells by HIV can occur via multiple mechanisms)
-lysis following HIV replication
-attack by HIV-specific cytotoxic CD8+ T lymphocytes
-natural killer cells
-antibody-dependent cellular cytotoxicity
-autoimmune process
-fusion of infected & uninfected cells
-apoptosis
102
HIV Prevention & Treatment
-No approved vaccine
-Many people infected are unaware
-Viruses on surfaces can be inactivated w/commercially available disinfectants & heat at 56 C for more than 30 minutes
-Knowledge of transmission greatest tool for control
-Use of condoms not 100% effective but have been shown to decrease transmission
-Avoidance of practices that favor HIV
102
How is HIV transmitted?
-sexual intercourse
-blood & blood products
-mother to infant
**bodily fluids**
102
The treatment for HIV is directed at "cocktails" of drugs. What is this combination?
Combination of reverse transcriptase inhibitors and protease inhibitors
-HAART
103
Reverse transcriptase inhibitors fall into these two categories:
*Nucleoside reverse transcriptase inhibitors
-AZT, D4T, & 3TC
*Non-Nucleoside reverse transcriptase inhibitors
-Nevirapine, efavirenz, & delavirdine
103
In regards to HIV treatment, how do protease inhibitors affect HIV replication?
Act late in HIV replication to prevent packaging of viral proteins
104
Prevention vaccine
-immunize uninfected individuals against disease
105
Therapeutic vaccine
-Boost immunity of those already infected
106
A successful vaccine must
-produce both mucosal & blood stream immunity
-get around HIV variability & stimulate cellular & humoral immunity
107
Rifamycins inhibit bacteria by:
A. Inhibiting DNA gyrase
B. Inhibiting RNA polymerase
C. Inhibiting folic acid synthesis
D. Interfering w/membrane integrity
B. Inhibiting RNA polymerase
108
Outside of living cells, viruses are:
A. scavenging glucose
B. slowly stockpiling ATP from mitochondria
C. Using cilia to move to the next host
D. Metabolically inert
D. Metabolically inert
109
The structure by ??? in T4 bacteriophage is:
A. tailspike
B. enelope
C. capsid
D. baseplate
C. capsid
110
The spike protein of a virus:
A. reverse transcribes RNA into DNA
B. facilitates attachment to host cells
C. integrates virus DNA into host genome
D. is important in volleyball tournaments
B. facilitates attachment to host cells
111
