Viral Genetics, Pathogenesis, Classification and Structure - Ornelles Flashcards
1
Q
Viruses are small. They are closer in size to __ than bacteria.
A
Viruses are small. They are closer in size to proteins than bacteria.
2
Q
Viruses have limited genetic capacity. They have no __ synthesis machinery.
A
Viruses have limited genetic capacity. They have no protein synthesis machinery.
3
Q
Viruses bring ___ not parts
A
instructions
4
Q
Progeny is formed in ___ – not by binary fission
A
bursts
5
Q
Genome is either __ or __. It evolves independently from the ___
A
RNA or DNA
host
6
Q
Viruses all have a __ protein – can be helical, cuboidal (icosahedral), or complex
A
capsid
7
Q
T/F: Not all viruses have a protein capsue, but the ones that infect humans do.
A
T
8
Q
Viruses have an optional ___ ___, which can be derived from the __, __ or the __.
A
Viruses have an optional lipid envelope, which can be derived from the plasma membrane, golgie or nuclear envelope
9
Q
Viral genomes are diverse. They can be __ or ___, can be single, doubl or partially double/singly stranded. Topology can be circular, linear or cross-linked. They can be a single segment or can be multiple.
A
RNA or DNA
10
Q
All viruses have a ___. The __ protects the viral genome. The __ mediates attachment to the cell if not enveloped (spike-like proteins on the surface of the naked virus often serve as the viral attachment protein. hey are often targeted by neutralizing ___). Sometimes, the capsid encapsulates ___ proteins.
A
All viruses have a capsid. This protects the viral genome. It mediates attachment to the cell if not enveloped (spike-like proteins on the surface of the naked virus often serve as the viral attachment protein. hey are often targeted by neutralizing ___). Sometimes the capsid encapsulated accessory proteins.
11
Q
Having an envelope typically renders a virion more ___ than a non-enveloped virion.
A
fragile
12
Q
___virus is the most common cause of the common cold. It is ___ stable –> no __ for attachment.
A
Rhinovirus is the most common cause of the common cold. It is environmentally stable –> no spikes for attachment
13
Q
Poliovirus is ___ sable.
A
environmentally
14
Q
___ corona virus can cause severe respiratory disease
A
SARS
15
Q
____ is the most common cause of CROUP in infants.
A
Parainfluenza virus (hPIV-1)
16
Q
___ is an orthomyxovirus with prominant ___ glycoproteins.
A
Influenza
spike
17
Q
___ is an envrionmentally stable RNA virus with segmented genome.
___ virus is an environmentally stable DNA virus.
A
Rota
Adeno
18
Q
HSV is a ____ with an ___capsid, with an envelop and __ proteins (unique to herpes)
A
dsDNA
icosahedral
tegument
19
Q
____ is a ssDNA and causes 5th disease (slapped cheek) and aplastic crsis (anemia)
A
Parvovirus
20
Q
___ is unusally stable –> large enveloped cirus
A
smallpox
21
Q
__ is a human retrovirus. It has spike glycoproteins and a distinctive capsid. It has an envelope.
A
HIV
22
Q
T/F: All viruses with a helical capsule have a lipid envelope
A
True
23
Q
What consequence does a lipid envelope have on a viruses stability?
A
It separates virion’s contents from environment and makes it unstable in dry environments.
24
Q
What maintains the lipid bilayer?
A
water - dehydration causes viral envelope integrity to be lost.
25
The obligate incracellular nature of virus intertwines viral replication with cellular processes. Host cell provides protein __ __ and ___
synthesis machinary
| energy
26
Small physical size of viruses requires them to adopt, simple, repeating elements for structure. They need to disassemble in the right environment requires a ___ structure.
metastable
27
Plaque assays determine infectious virusin a sample that can proceed through multiple rounds of replication. It is based on the ___ effect
cytopathic
28
__ test: cells fuse together when infected with parainfluenza virus. This causes a cytopathic effect --> multinucleated giant cells. __ test helps you see this. Use in herpes virus identification
Tzanck
29
All RNA viruses must direct expression of RdRP
| T or F
T
30
__ and __ viruses must bring RdRP so that it can get started with protein translation
negative ssRNA and dsDNA
31
Rhinovirus escapes neutrialization AB's by ___ ___. Changes occur on the __ Of the capsid to escape AB recognition. It has generated over __ serotypes. Invariant canyon allows virus to bind host cell receptor, while AB's have trouble targeting the capside because of the constant change.
Rhinovirus escapes neutrialization AB's by antigenic drift. Changes occur on the surface of the capsid to escape AB recognition. It has generated over 100 serotypes. Invariant canyon allows virus to bind host cell receptor, while AB's have trouble targeting the capside because of the constant change.
32
Antigenic shift:
Influenza A has __ segments. Segments PA and PB2 encode for __ and __. Changes in these proteins increase constantly evolving ___
Influenza A has 8 segments. Segments PA and PB2 encode for HA and NA. Changes in these proteins increase constantly evolving strains.
33
In __ __, antigens expressed by virus has undergone not a small shift from one amino acid, to the other, but a wholesale shift. It happens because 2 segments that encode for HA and NA are switched. This occurs, because influenza, for ecample, can infect multiple hosts. Viruses from different species have the ability to enter a permissible human host. For example, the human virus can acquire some gene segments from a duck influenza virus and mix it with human virus. If the newly recombined virus can survive, the human population is not prepared for dealing with the massive number of changes. This is the origin of ____ and ___ forms of the influenza virus.
In antigenic shift, antigens expressed by virus has undergone not a small shift from one amino acid, to the other, but a wholesale shift. It happens because 2 segments that encode for HA and NA are switched. This occurs, because influenza, for ecample, can infect multiple hosts. Viruses from different species have the ability to enter a permissible human host. For example, the human virus can acquire some gene segments from a duck influenza virus and mix it with human virus. If the newly recombined virus can survive, the human population is not prepared for dealing with the massive number of changes. This is the origin of epidemic and pandemic forms of the influenza virus.
34
DNA viral genomes can recombine by breaking and rejoining. BUT cells must be infected with __ different ___.
2 different viruses
35
Recombination of "copy choice" is a unique characteristic of RNA viruses. All must be infected with __ distinct genomes. Start with one __ and the hop to another. This is very common amongst ___ viruses, as much as 20% of poliovirus RNA's undergo copy choice.
Some diploid retroviruses can use copy choice recombination. Recombination can "rescue" defective viruses. It can also introduce deletion in viral genome.
Recombination of "copy choice" is a unique characteristic of RNA viruses. All must be infected with 2 distinct genomes. Start with one RNA and the hop to another. This is very common amongst +ssRNA viruses, as much as 20% of poliovirus RNA's undergo copy choice.
Some diploid retroviruses can use copy choice recombination. Recombination can "rescue" defective viruses. It can also introduce deletion in viral genome
36
Non-genetic changes such as __ and __.
___ - permits propagation of a defective virus -- host cell genome may provide the missing gene product.
If you can infect a cell with 2 viruses, wild type and defective genome, the defective genome will not be able to replicate. However, the cell still has the wild type gene, which has the necesarry resources to copy the defective gene, resulting in progeny with both wile type and defective.
___ - presence of 2 viruses in same cell interferes with each other. Result is that the presence of one genome precludes amplification of the other genome. YOu end up only seeing one genotype of the infection. This was significant in the polio vaccine.
Non-genetic changes such as complementation and interference.
Complementation- permits propagation of a defective virus -- host cell genome may provide the missing gene product.
If you can infect a cell with 2 viruses, wild type and defective genome, the defective genome will not be able to replicate. However, the cell still has the wild type gene, which has the necesarry resources to copy the defective gene, resulting in progeny with both wile type and defective.
Interference- presence of 2 viruses in same cell interferes with each other. Result is that the presence of one genome precludes amplification of the other genome. YOu end up only seeing one genotype of the infection. This was significant in the polio vaccine.
37
Non-genetic changes - ___ mixing aka ____.
| This is used to construct viral vectors with different attachment proteins.
Non-genetic changes - transcapsidation phenotypic mixing.
| This is used to construct viral vectors with different attachment proteins.
38
The sum of effects on host due to ___ and ___
viral determinants and host immune response
1. Viral determinants
- initial innoculum - size is important. too small? nothing happens
- site of infection/tropism
- capactiy to invade secondary tissue
- cytopathicity --> propensity of virus to cause cell death and the cytopathic effect
2. Host resposne
- CD8 T cell damage
- CD4 inflammation response
-Antibody mediated damage
ROS
39
Potential outcomes of viral infections?
1. abortive of failed --> due to __ or __ ___
2. __ or ___ --> person is infected and virus grow and replicated but no ___. This is a __ situation for the virus because it spreads w/o causing problems
3. __ __ --> virus levels rise over time to the point where disease is evident. Immune system resolves infection and everything goes back to normal
4. __ __ --> virus enters, replicated and may or may not cause disease. This may last for a long time. Ultimately, there is some degradation in the hsot that leads to the manifestation of a disease state. Example __ and ___
5.__, __ infetction --> virus successfully infects and spread, presents as acute disease, and then there is a period where there is no disease with no virus present. Periodically, virus can reemerge with or without symptoms.
It can also re emerge and cause more serious disease and sometimes death.
Example is HIV and HTLV and herpes.
Potential outcomes of viral infections?
1. abortive of failed --> due to IS or failed virus
2. subclinical or inapparent --> person is infected and virus grow and replicated but no symptoms. This is a beneficial situation for the virus because it spreads w/o causing problems
3. acute infection --> virus levels rise over time to the point where disease is evident. Immune system resolves infection and everything goes back to normal
4. persistent infection --> virus enters, replicated and may or may not cause disease. This may last for a long time. Ultimately, there is some degradation in the hsot that leads to the manifestation of a disease state. Example __ and ___
5. latent, reactivating infection --> virus successfully infects and spread, presents as acute disease, and then there is a period where there is no disease with no virus present. Periodically, virus can reemerge with or without symptoms.
It can also re emerge and cause more serious disease and sometimes death.
Example is HIV and HTLV and herpes.
40
Role of virus entry influences sites of viral replication:
Localized to URT - numerous viruses do this.
Localized to LRT - __, __, __, __
Systemic from RT: enters through respiratory tract, replicate in epithelial or related cells ad spread throughout body. Examples are __, ___, __ ,___ and __
Role of virus entry influences sites of viral replication:
Localized to URT - numerous viruses do this.
Localized to LRT - RSV, INfluenza A and B, parainfluenza virus
Systemic from RT: enters through respiratory tract, replicate in epithelial or related cells ad spread throughout body. Examples areRubella, arenavirus, mumps, measles, VZV
41
Stable viruses?
RRAPS
| Rhino, Rota, Adena, Polio, Smallpox
42
• Historical classification is based on __, ___, genome, geography, or ____ mechanism
• Historical classification is based on disease, appearance, genome, geography, or transmission mechanism
43
• Biological classification is based on genetic sequence (evolutionary relatedness), serotype & Baltimore shared challenges in creating mRNA (dsDNA->mRNA, ssDNA made to dsDNA by host repair enzymes 1st, +ssRNA=mRNA, -ssRNA and dsRNA carry RNA pol with them, dsDNA and ssRNA RTs)
• Biological classification is based on genetic sequence (evolutionary relatedness), serotype & Baltimore shared challenges in creating mRNA (dsDNA->mRNA, ssDNA made to dsDNA by host repair enzymes 1st, +ssRNA=mRNA, -ssRNA and dsRNA carry RNA pol with them, dsDNA and ssRNA RTs)
44
• ____ genome replication is unique among viruses
• RNA genome replication is unique among viruses
45
• __ genome can be treated as host intact (ds, circular) or _____ (ss, linear) genome, but virus needs to ___ DNA synthesis in a quiescent cell
• DNA genome can be treated as host intact (ds, circular) or damaged (ss, linear) genome, but virus needs to mobilize DNA synthesis in a quiescent cell
46
• Metastable genome allows ___ in right environment for replication
• Metastable genome allows disassembly in right environment for replication
47
• Viral envelope has a ___ __ ___ (lipid bilayer) with integrity maintained by water: renders virion susceptible to inactivation by dehydration, can come from PM, NM, or Golgi membrane
• Viral envelope has a fluid mosaic model (lipid bilayer) with integrity maintained by water: renders virion susceptible to inactivation by dehydration, can come from PM, NM, or Golgi membrane
48
• ___ ___ surface proteins are found on naked (attachment, Ab target) and enveloped (glycoproteins, attachment (e.g., HA), Ab target) viruses
• Spike-like surface proteins are found on naked (attachment, Ab target) and enveloped (glycoproteins, attachment (e.g., HA), Ab target) viruses
49
• _____ can block unique proteins or processes in viruses: viral pol for replication, viral protein used to permit H+ entry (M2), proteases, nuclease that degrades cell mRNA
• Antivirals can block unique proteins or processes in viruses: viral pol for replication, viral protein used to permit H+ entry (M2), proteases, nuclease that degrades cell mRNA
50
• Seven steps in viral replication include:
```
• Seven steps in viral replication include attachment
entry
uncoating
expression of viral genome
replication of genome
assembly of progeny
release and maturation
```
51
• Attachment after overcoming physical barriers includes viral protein-host receptor specificity and is dynamic (low affinity-____ to host cell, high affinity-at the right host cell/tropism and further actions via co-receptors)
• Attachment after overcoming physical barriers includes viral protein-host receptor specificity and is dynamic (low affinity-proximity to host cell, high affinity-at the right host cell/tropism and further actions via co-receptors)
52
• Entry most common via ___ ____ ___ (but need to deal with endosome acidity or lysosome fusion), and often coupled with uncoating (and fusion of enveloped viruses) at PM or endosome, (can rely on acidification—e.g., influenza M2 ion channels), or NM (adenovirus mobile histone H1 & nuclear import pathway/pore)
• Entry most common via receptor-mediated endocytosis (but need to deal with endosome acidity or lysosome fusion), and often coupled with uncoating (and fusion of enveloped viruses) at PM or endosome, (can rely on acidification—e.g., influenza M2 ion channels), or NM (adenovirus mobile histone H1 & nuclear import pathway/pore)
53
• Gene expression for RNA and DNA of early proteins (activators, effectors, replication enzymes, host cell regulating) ____, before late proteins (mostly large amounts of structural proteins)
• Gene expression for RNA and DNA of early proteins (activators, effectors, replication enzymes, host cell regulating) first before late proteins (mostly large amounts of structural proteins)
54
• DNA pol displays high fidelity d/t template (1 in ____) while RNA errors more common d/t lack of proofreading w/ RNA pol (1 in 1____, quasi-species w/ each progeny unique, only in RNA viruses and most non-viable)
• DNA pol displays high fidelity d/t template (1 in 10^8-11) while RNA errors more common d/t lack of proofreading w/ RNA pol (1 in 10^3-5, quasi-species w/ each progeny unique, only in RNA viruses and most non-viable)
55
```
• Gene expression and replication for DNA viruses can be understood by the properties of 4 groups:
very typical (relies on viral DNA genome),
very small (dependent on host DNA synthesis to “repair” viral ssDNA to ds),
very large (replicates in cytoplasm independently-Pox synthesizes it’s own viral DNA pol),
very strange (HBV RT feature)
```
• Gene expression and replication for DNA viruses can be understood by the properties of 4 groups: very typical (relies on viral DNA genome), very small (dependent on host DNA synthesis to “repair” viral ssDNA to ds), very large (replicates in cytoplasm independently-Pox synthesizes it’s own viral DNA pol), and very strange (HBV RT feature)
56
• +ssRNA naked viruses are immediately ___ (seen as mrNA, translated into proteins fast) which is why protease inhibitors are great for them (block cleaving of polyprotein), but not true for –ssRNA viruses
• +ssRNA naked viruses are immediately infectious (seen as mrNA, translated into proteins fast) which is why protease inhibitors are great for them (block cleaving of polyprotein), but not true for –ssRNA viruses
57
• In assembly, simple icosahedral and helical nucleocapsid self-assemble, and bud at PM at the ___ (move out through lungs, gut) or ___ (move in through blood) surfaces
• In assembly, simple icosahedral and helical nucleocapsid self-assemble, and bud at PM at the apical (move out through lungs, gut) or basolateral (move in through blood) surfaces
58
• Release and maturation may or may not __/___ cell, and may include acquiring an ___ and proteolytic processing
• Release and maturation may or may not kill/lyse cell, and may include acquiring envelope and proteolytic processing
59
• Viral assays exploit steps in viral expression or replication: viral NA (PCR, LCR), proteins (IF microscopy, serological methods-Western blot-identifies Ag by size and reaction to a specific Ab, ELISA), enzymes (ELISA-indirect or sandwich Ag capture, Ab capture), cytopathic effect (cell fusion, Tzanck test, plaque-quantifies low amounts of infectious virus), particles/morphology (electron microscopy, RTase assay), or Ab (Hemagglutination inhibition test-RBCs collect at bottom if virus doesn’t have protein to identify viruses that bind sialic acid, serology)
• Viral assays exploit steps in viral expression or replication: viral NA (PCR, LCR), proteins (IF microscopy, serological methods-Western blot-identifies Ag by size and reaction to a specific Ab, ELISA), enzymes (ELISA-indirect or sandwich Ag capture, Ab capture), cytopathic effect (cell fusion, Tzanck test, plaque-quantifies low amounts of infectious virus), particles/morphology (electron microscopy, RTase assay), or Ab (Hemagglutination inhibition test-RBCs collect at bottom if virus doesn’t have protein to identify viruses that bind sialic acid, serology)
60
• Viral proteins detected with assays: e.g., fluorescent Ab test (direct or indirect) for ____nucleocapsid protein
• Viral proteins detected with assays: e.g., fluorescent Ab test (direct or indirect) for rabies nucleocapsid protein
61
• Cytopathic effect of virus can be used to detect (assay): cell ___ (parainfluenza), _____ smear for MGCs (herpes)
• Cytopathic effect of virus can be used to detect (assay): cell fusion (parainfluenza), Tzanck smear for MGCs (herpes)
62
• _____ detects/measures DNA: end-point shows saturation of products (can quantify infectious virus across a wide concentration range), real-time quantifies viral nucleic acid
• PCR detects/measures DNA: end-point shows saturation of products (can quantify infectious virus across a wide concentration range), real-time quantifies viral nucleic acid
63
• ____ virus challenge is getting to nucleus, while ___ viruses must carry or encode for RNA pol & face low fidelity
• DNA virus challenge is getting to nucleus, while RNA viruses must carry or encode for RNA pol & face low fidelity
64
• Heritable changes include point mutations (physical insults, pol error), insertions/deletions (physical insults, pol errors, pol copy-choice-jumping to other site of same virus RNA), and recombination events (segment reassortment, breakage and rejoining/DNA crossover of 2 different viruses-e.g., adenovirus, pol copy choice/jumping to different virus RNA-e.g., enteroviruses or diploid RT viruses)
• Heritable changes include point mutations (physical insults, pol error), insertions/deletions (physical insults, pol errors, pol copy-choice-jumping to other site of same virus RNA), and recombination events (segment reassortment, breakage and rejoining/DNA crossover of 2 different viruses-e.g., adenovirus, pol copy choice/jumping to different virus RNA-e.g., enteroviruses or diploid RT viruses)
65
•___ ___ (point mutations to Ab-binding sites) occurs in rhinovirus (capsid surface) and influenza virus (HA, NA) to escape Ab recognition (e.g., why influenza B immunity diminishes over time, people are re-infected with rhinovirus (cold))
• Antigenic drift (point mutations to Ab-binding sites) occurs in rhinovirus (capsid surface) and influenza virus (HA, NA) to escape Ab recognition (e.g., why influenza B immunity diminishes over time, people are re-infected with rhinovirus (cold))
66
• ___ ___in influenza A by recombination (reassortment of segmented genome, swaps HA and NAs) - pandemics
• Antigenic shift in influenza A by recombination (reassortment of segmented genome, swaps HA and NAs) - pandemics
67
• Non-genetic changes include _____ (host provides solution for missing/defective gene product), _____ (one viral genome shuts down the other present virus’ genome, incl. vaccine genomes), and ___ ___ (transcapsidation, progeny from different viruses mix/match attachment proteins)
• Non-genetic changes include complementation (host provides solution for missing/defective gene product), interference (one viral genome shuts down the other present virus’ genome, incl. vaccine genomes), and phenotype mixing (transcapsidation, progeny from different viruses mix/match attachment proteins)
68
• Live attenuated are ____ sensitive vaccines passed through animal cells repeatedly to _____ virulence and introduce point mutations to do so (Sabin polio, FluMist, yellow fever), while non-attenuated delivered to tissue where it doesn’t cause disease (adenovirus)
• Live attenuated are temperature sensitive vaccines passed through animal cells repeatedly to decrease virulence and introduce point mutations to do so (Sabin polio, FluMist, yellow fever), while non-attenuated delivered to tissue where it doesn’t cause disease (adenovirus)
69
• ____ vaccines pair a sub-virion component of the virus with an adjuvant (inflammatory signal) and result in high Ab response but little cellular immunity (HBV, HPV), less common/approved than live/attenuated viruses
• Subunit vaccines pair a sub-virion component of the virus with an adjuvant (inflammatory signal) and result in high Ab response but little cellular immunity (HBV, HPV), less common/approved than live/attenuated viruses
70
• ____ vaccines are delivered with adjuvant and require multiple shots (Salk polio, polyoma)
• Killed/inactivated vaccines are delivered with adjuvant and require multiple shots (Salk polio, polyoma)
71
• Pathogenesis includes viral (initial inoculum, infection site, tropism, invasive capacity, cytopathicity) and host response (CD8 killing, CD4 TH1 inflammation, Ab-mediated damage, ROS), and dx outcome is dependent on host-virus interactions
• Pathogenesis includes viral (initial inoculum, infection site, tropism, invasive capacity, cytopathicity) and host response (CD8 killing, CD4 TH1 inflammation, Ab-mediated damage, ROS), and dx outcome is dependent on host-virus interactions
72
• Viral infection can result in viral ____ (failed, abortive, most common outcome), survival with clearance that provides durable or transient immunologic memory or enhances a 2nd infection (____l-replicating virus not detected, acute), or survival with chronic infection that has continuous low levels of replication (___) or potential to restart replication (__/____)
• Viral infection can result in viral death (failed, abortive, most common outcome), survival with clearance that provides durable or transient immunologic memory or enhances a 2nd infection (subclinical-replicating virus not detected, acute), or survival with chronic infection that has continuous low levels of replication (persistent) or potential to restart replication (latent/reactivating)
73
• A rare outcome of viral infection is ___ into host genome by a defective virus, expression of cancer-causing genes
• A rare outcome of viral infection is integration into host genome by a defective virus, expression of cancer-causing genes
74
• Virus spreads locally/cell-to-cell where it replicates at site of entry (e.g., skin or respiratory epithelium), and systemically through regional lymph nodes leading to primary ____ and access to central lymphoid or other organs, ____ viremia (e.g., polio, hep C, HIV measles)
• Virus spreads locally/cell-to-cell where it replicates at site of entry (e.g., skin or respiratory epithelium), and systemically through regional lymph nodes leading to primary viremia and access to central lymphoid or other organs, secondary viremia (e.g., polio, hep C, HIV measles)
75
• Systemic spread can be cell-associated and avoid viremia (e.g., measles), and others that are transmitted fecal-orally and can resist degradation in GI (acid resistant viral capsid) can cause viremia and death of neurons (polio)
• Systemic spread can be cell-associated and avoid viremia (e.g., measles), and others that are transmitted fecal-orally and can resist degradation in GI (acid resistant viral capsid) can cause viremia and death of neurons (polio)
76
• Spread of neural infections occur via ___nerves (herpes 1 and 2, rabies) or compromised BBB (West Nile)
• Spread of neural infections occur via peripheral nerves (herpes 1 and 2, rabies) or compromised BBB (West Nile)
77
• Pathology (dx, symptoms) related to replication in target organs: rashes (capillary endothelium/skin), coryza (nasal epithelium), CNS inflammation, flaccid paralysis (motor neurons or ventral horn), hepatitis, immunodeficiency (lymphoid organs), myocarditis, orchitis, cancer or warts (cervical epithelium), etc.
• Pathology (dx, symptoms) related to replication in target organs: rashes (capillary endothelium/skin), coryza (nasal epithelium), CNS inflammation, flaccid paralysis (motor neurons or ventral horn), hepatitis, immunodeficiency (lymphoid organs), myocarditis, orchitis, cancer or warts (cervical epithelium), etc.
78
• Infected host cell death is a frequent outcome (cytopathic effect) and includes apoptosis, killing by immune cell, lysis (e.g., viral-mediated killing of host important in paralytic polio and HIV immune suppression pathology, while immune-mediated cell killing plays a role in EBV mono and hep B chronic hepatitis pathology)
• Infected host cell death is a frequent outcome (cytopathic effect) and includes apoptosis, killing by immune cell, lysis (e.g., viral-mediated killing of host important in paralytic polio and HIV immune suppression pathology, while immune-mediated cell killing plays a role in EBV mono and hep B chronic hepatitis pathology)
79
• The non-specific innate players (Day 1-4) against viruses include epithelial cells, macrophages, and DCs (IFN 1, cytokines), followed closely by NKs (kill cells missing HCI I self-marker), and neutrophils (phagocytic principle responder), systemic pathology can result with a huge innate immune response (e.g., influenza A)
• The non-specific innate players (Day 1-4) against viruses include epithelial cells, macrophages, and DCs (IFN 1, cytokines), followed closely by NKs (kill cells missing HCI I self-marker), and neutrophils (phagocytic principle responder), systemic pathology can result with a huge innate immune response (e.g., influenza A)
80
• The specific adaptive response players (Day 4-10) against viruses include CD8s (IFNg and cell lysis) and CD4 TH1s (IFNg and stimulating CD8s), followed later by B cells (neutralizing Abs)
• The specific adaptive response players (Day 4-10) against viruses include CD8s (IFNg and cell lysis) and CD4 TH1s (IFNg and stimulating CD8s), followed later by B cells (neutralizing Abs)
81
• _____ (non-infected cells) can cause dx because infected cells release toxins that change their fx (e.g., _____ infected cells secrete NSP4 toxin that causes increased Cl- secretion leading to watery diarrhea)
• Bystander (non-infected cells) can cause dx because infected cells release toxins that change their fx (e.g., Rotavirus infected cells secrete NSP4 toxin that causes increased Cl- secretion leading to watery diarrhea)
82
• Viruses can alter the fx of non-infected immune cells and cause dx (measles suppression of T cells)
• Viruses can alter the fx of non-infected immune cells and cause dx (measles suppression of T cells)
