Dr Iqbal Class 01 Lec 01 Flashcards
1
Q
How do pathogens exploit epithelial barriers to establish endogenous infections and what specific mechanisms do they use to overcome these barriers?
A
Pathogens exploit epithelial barriers by causing aberrations that allow endogenous infections. They use adhesins for specific attachment
2
Q
What role does the specificity of adhesins play in the colonization of epithelial surfaces by pathogens like H. pylori?
A
Adhesins enable specific binding to epithelial cell receptors
3
Q
How does Bordetella toxin disrupt host cell function without entering the cell and what are the implications for host defense?
A
Bordetella toxin disrupts host cell signaling by ADP-ribosylation of G-proteins
4
Q
What is the significance of pedestal formation by EPEC in the context of extracellular pathogenesis?
A
EPEC induces pedestal formation by injecting effector proteins via a type III secretion system
5
Q
Why do intracellular pathogens prefer niches within host cells and how do these niches provide advantages over extracellular environments?
A
Intracellular pathogens favor host cell niches for nutrient access
6
Q
How do bacteria and protozoa differ from viruses in their intracellular replication strategies?
A
Bacteria and protozoa replicate in the cytosol or membrane-enclosed compartments
7
Q
What evolutionary advantage do DNA viruses gain by replicating in the host cell nucleus?
A
DNA viruses replicate in the nucleus to utilize host DNA and RNA polymerases for genome replication and transcription
8
Q
Why do RNA viruses encode their own replication enzymes and how does this influence their replication site?
A
RNA viruses encode replication enzymes because host cells lack RNA-dependent RNA polymerases. This necessitates cytoplasmic replication
9
Q
How does the retroviral enzyme reverse transcriptase facilitate the unique replication strategy of retroviruses?
A
Reverse transcriptase converts retroviral RNA into DNA in the cytoplasm
10
Q
What is the significance of receptor specificity in preventing cross-species viral infections and how do mutations alter this barrier?
A
Receptor specificity restricts viral host range by requiring precise receptor-ligand interactions. Mutations altering receptor binding
11
Q
How does the use of multiple receptor types by HIV influence its pathogenesis over the course of infection?
A
HIV initially uses CCR5 to infect macrophages
12
Q
What structural features distinguish a virion from a virus and how do these features contribute to infectivity?
A
A virion is the complete
13
Q
How do glycoproteins on viral surfaces facilitate host cell entry and what role does glycosylation play in this process?
A
Glycoproteins bind host receptors
14
Q
What is the role of gangliosides in viral attachment and how do their sialic acid components contribute to this process?
A
Gangliosides
15
Q
How do the sialic acid binding sites of influenza A virus hemagglutinin and neuraminidase differ in function and why are these differences critical for viral life cycle?
A
Hemagglutinin binds sialic acid for host cell entry
16
Q
What is the mechanistic similarity between viral envelope fusion and SNARE protein-mediated vesicle docking and how does this facilitate viral entry?
A
Both involve protein-mediated membrane fusion
17
Q
How does macropinocytosis differ from clathrin-coated pit endocytosis in the context of viral entry and what advantages does it offer to certain viruses?
A
Macropinocytosis involves large
18
Q
What are the four distinct viral entry strategies illustrated in Figure 23-18 and how do they differ in their mechanisms?
A
1) HIV fuses with plasma membrane; 2) Influenza fuses post-endocytosis; 3) Poliovirus forms pores in endosomes; 4) Adenovirus disrupts endosomes
19
Q
How does the zipper mechanism of bacterial invasion differ from phagocytosis in non-phagocytic cells and what specific proteins are involved?
A
The zipper mechanism involves invasion proteins like invasin binding host receptors (e.g.
20
Q
What is the role of the type III secretion system in the trigger mechanism of bacterial invasion and how does it manipulate host cell cytoskeletal dynamics?
A
The type III secretion system injects effector proteins that activate Rho GTPases and Arp2/3
21
Q
How does Yersinia pseudotuberculosis utilize the invasin protein to mimic fibronectin and invade host cells?
A
Invasin contains an RGD motif
22
Q
What is the significance of Listeria monocytogenes targeting E-cadherin for host cell invasion and how does this affect tissue specificity?
A
E-cadherin binding by Listeria’s invasion protein restricts invasion to epithelial cells expressing this junctional protein
23
Q
How do effector proteins injected by Salmonella enterica through the type III secretion system reorganize the host cytoskeleton and what visual evidence supports this?
A
Effector proteins activate Rho GTPases
24
Q
What are the molecular differences between the trigger and zipper mechanisms of bacterial invasion as depicted in Figure 23-19?
A
The zipper mechanism uses invasion proteins binding receptors like integrins
25
How does the influenza virus exploit sialic-acid-containing oligosaccharides for host cell attachment and why are these receptors advantageous?
Influenza’s hemagglutinin binds abundant sialic-acid oligosaccharides on host cells
26
Why does the rabies virus specifically target the nicotinic acetylcholine receptor and what are the implications for its pathogenesis?
The rabies virus binds nicotinic acetylcholine receptors to infect neurons
27
How do chemokine receptor ligands like Rantes and Sdi1 inhibit HIV infection and what does this suggest about co-receptor function?
Rantes and Sdi1 block CCR5 and CXCR4
28
What is the significance of the smallpox virus encoding its own DNA replication machinery and how does this differ from typical DNA viruses?
Smallpox replicates in the cytoplasm using its own DNA polymerase
29
How do enveloped viruses like HIV achieve genome release into the host cytosol and what challenges do they face during this process?
HIV fuses its envelope with the plasma membrane
30
What is the role of the Arp2/3 complex in bacterial invasion via the trigger mechanism and how does it contribute to membrane ruffling?
The Arp2/3 complex nucleates actin filaments
31
How does the receptor-mediated endocytosis pathway used by influenza differ from the pore-forming strategy of poliovirus and what are the implications for their respective infections?
Influenza fuses with endosomal membranes post-endocytosis
32
Why do adenoviruses disrupt endosomal membranes rather than fuse with them and how does this strategy align with their nuclear replication requirements?
Adenoviruses disrupt endosomes to release their capsid
33
What are the benefits of intracellular pathogens escaping antibodies and how does this influence their persistence in the host?
Escaping antibodies prevents neutralization
34
How does the structure of the GM1 ganglioside contribute to its role as a viral receptor and what specific components are critical for this function?
GM1’s glycosphingolipid structure
35
What is the significance of the hemagglutinin-esterase-fusion (HEF) protein in influenza C virus and how does it compare to influenza A’s hemagglutinin and neuraminidase?
HEF combines attachment (sialic acid binding) and release (esterase activity) functions
36
How do non-enveloped viruses like poliovirus achieve genome release without an envelope and what challenges does this pose compared to enveloped viruses?
Poliovirus forms pores in endosomal membranes to extrude its RNA
37
What is the role of the Rho family of small GTPases in bacterial invasion and how do they bridge the zipper and trigger mechanisms?
Rho GTPases regulate actin polymerization
38
How does the integration of retroviral dsDNA into the host genome provide a long-term advantage for viral persistence?
Integration allows retroviruses to persist as proviruses
39
What is the significance of the crystal structures (1MQM
1W20
40
How does the Salmonella pathogenicity island 1 (SPI1) contribute to the trigger mechanism and what specific host cell changes does it induce?
SPI1 encodes the type III secretion system
41
What is the evolutionary significance of viruses carrying small genomes and how does this relate to their dependence on host machinery?
Small genomes reduce replication costs
42
How does the binding of invasin to β1 integrins mimic natural host cell processes and what does this suggest about bacterial adaptation?
Invasin mimics fibronectin’s RGD motif
43
Why do some viruses use multiple entry strategies and how does this flexibility impact their infectivity across different cell types?
Multiple entry strategies (e.g.
44
What is the role of clathrin-coated pits in viral entry and how does their specificity compare to macropinocytosis?
Clathrin-coated pits facilitate receptor-mediated endocytosis
45
How does the trigger mechanism’s induction of membrane ruffling resemble macropinocytosis and what advantages does this provide to bacteria like Salmonella?
Membrane ruffling mimics macropinocytosis by forming actin-driven protrusions that engulf bacteria. This allows Salmonella to invade non-phagocytic cells efficiently
46
What is the significance of the actin-rich ruffles observed in fluorescence micrographs during Salmonella invasion and how do they confirm the trigger mechanism?
Actin-rich ruffles
47
How does the influenza A virus’s hemagglutinin trimer structure contribute to its receptor-binding efficiency and what does the yellow coloring in Figure 12 indicate?
The hemagglutinin trimer’s multiple binding sites enhance sialic acid attachment efficiency. Yellow coloring in Figure 12 highlights receptor-binding sites
48
What is the role of the catalytic site of neuraminidase in influenza A virus and how does its green coloring in Figure 12 differentiate it from receptor-binding sites?
The neuraminidase catalytic site
49
How does the adenovirus’s strategy of docking onto nuclear pores after endosomal disruption optimize its replication cycle?
Docking at nuclear pores allows direct DNA delivery to the nucleus
50
What is the significance of the 1918 influenza pandemic’s high mortality and how does its avian gene origin inform our understanding of zoonotic transmission?
The 1918 pandemic’s 675
51
How does the HIV fusion process depicted in Figure 23-20 provide insights into its entry efficiency and what are the limitations of electron microscopy in capturing this process?
Electron micrographs show HIV’s envelope fusing with the plasma membrane
52
What is the role of formins in the trigger mechanism of bacterial invasion and how do they interact with other cytoskeletal elements?
Formins nucleate actin filaments
53
How does the specificity of viral receptors act as a barrier to cross-species transmission and what specific example illustrates this?
Receptor specificity limits viral host range
54
What is the significance of the nicotinic acetylcholine receptor’s role in rabies virus infection and how does it influence the virus’s tissue tropism?
The nicotinic acetylcholine receptor restricts rabies to neurons
55
How does the integration of retroviral DNA into the host genome as described for retroviruses provide a mechanism for latency?
Integration allows retroviruses to remain dormant as proviruses
56
What is the role of the WASP protein in the trigger mechanism of bacterial invasion and how does it interact with the Arp2/3 complex?
WASP activates Arp2/3
57
How does the smallpox virus’s cytoplasmic replication strategy provide an advantage over nuclear-replicating DNA viruses?
Cytoplasmic replication avoids nuclear transport
58
What is the significance of the chemokine receptors CCR5 and CXCR4 in HIV’s evolving tropism and how do their natural ligands influence infection?
CCR5 enables macrophage infection early
59
How does the structure of the influenza C virus’s HEF protein streamline its infection process compared to influenza A?
HEF’s dual role in sialic acid binding and cleavage reduces the need for separate proteins like influenza A’s hemagglutinin and neuraminidase
60
What is the role of the RGD motif in Yersinia’s invasin protein and how does it mimic host cell adhesion processes?
The RGD motif mimics fibronectin’s integrin-binding site
61
How does the trigger mechanism’s use of the SPI1 type III secretion system differ from the zipper mechanism’s reliance on invasion proteins?
SPI1 injects effectors to induce broad cytoskeletal ruffling
62
What is the significance of the actin filament labeling in fluorescence micrographs of Salmonella invasion and how does it confirm the trigger mechanism’s mechanism?
Red-labeled actin filaments surrounding yellow Salmonella in micrographs confirm actin polymerization driven by the trigger mechanism
63
How does the pore-forming strategy of poliovirus differ from the membrane disruption strategy of adenovirus and what are the implications for their respective infections?
Poliovirus forms pores for RNA release
64
What is the role of the sialic acid moiety in the binding sites of influenza A’s hemagglutinin and neuraminidase as shown in Figure 12 and how does it influence antiviral design?
Sialic acid moieties mediate attachment and release. Their structural role in binding sites informs inhibitors like oseltamivir
65
How does the 1957 influenza pandemic’s estimated 116000 US deaths reflect its pathogenicity and what role did avian genes play in its emergence?
The 1957 pandemic’s mortality reflects reassortment with avian genes
66
What is the significance of the electron micrograph in Figure 23-20 for understanding HIV entry and what are its limitations in capturing dynamic processes?
The micrograph shows HIV’s envelope fusion
67
What is the role of formins in the trigger mechanism of bacterial invasion and how do they contribute to its efficiency?
Formins nucleate linear actin filaments
68
What is the significance of the chemokine receptor ligands Rantes Mip1α and Mip1β in blocking HIV infection and how do they inform therapeutic strategies?
These ligands block CCR5
69
How does the influenza C virus’s HEF protein’s dual role in attachment and release provide an evolutionary advantage over influenza A’s separate proteins?
HEF’s combined functions reduce genome size and protein complexity
70
What is the role of the E-cadherin receptor in Listeria’s invasion and how does its specificity influence the bacterium’s tissue tropism?
E-cadherin binding restricts Listeria to epithelial cells
71
How does the SPI1 type III secretion system’s induction of actin-rich ruffles mimic macropinocytosis and what advantages does this provide?
SPI1 effectors induce actin ruffles resembling macropinocytosis
72
What is the significance of the green-colored catalytic sites in Figure 12 and how do they contribute to influenza’s viral release?
Green catalytic sites on neuraminidase cleave sialic acid
73
How does the 2009 H1N1 pandemic’s lower mortality (12500 US deaths) compared to 1918 reflect changes in viral pathogenicity or host factors?
Lower mortality in 2009 reflects milder pathogenicity due to partial immunity from prior H1N1 exposure and improved medical interventions
74
What is the limitation of electron microscopy in capturing the HIV fusion process in Figure 23-20 and how could complementary techniques address this?
Electron microscopy provides static images
75
How does the trigger mechanism’s activation of formins and Rho GTPases contribute to its efficiency in bacterial invasion?
Formins and Rho GTPases synergize to nucleate and stabilize actin filaments
76
What is the role of the Arp2/3 complex in both the zipper and trigger mechanisms and how does its activation differ between the two?
Arp2/3 nucleates actin in both mechanisms. In the zipper mechanism
77
How does the influenza virus’s use of abundant sialic-acid-containing oligosaccharides provide a strategic advantage for its infectivity?
Abundant sialic acid receptors enable influenza to infect diverse cell types
78
What is the significance of the nuclear pore docking strategy of adenovirus and how does it optimize its replication cycle?
Docking at nuclear pores ensures direct DNA delivery to the nucleus
79
How does the integration of retroviral dsDNA into the host genome provide a mechanism for immune evasion?
Integration as a provirus shields retroviruses from immune detection
80
What is the role of the WASP protein in the cytoskeletal dynamics of the trigger mechanism and how does it interact with Rho GTPases?
WASP links Rho GTPase signaling to Arp2/3 activation
81
How does the smallpox virus’s encoding of its own DNA polymerase provide a replication advantage and what are the trade-offs?
Encoding DNA polymerase enables cytoplasmic replication
82
What is the significance of the chemokine receptor CXCR4 in HIV’s late-stage infection and how does its ligand Sdi1 influence viral entry?
CXCR4 enables T-cell infection
83
How does the influenza C virus’s HEF protein’s dual functionality provide an evolutionary advantage over influenza A’s separate proteins?
HEF’s combined attachment and release functions reduce genome size and protein complexity
84
What is the role of the E-cadherin receptor in Listeria’s tissue-specific invasion and how does it influence the bacterium’s pathogenicity?
E-cadherin binding targets epithelial cells
85
How does the SPI1 type III secretion system’s induction of actin-rich ruffles contribute to Salmonella’s broad host cell range and what visual evidence supports this?
SPI1-induced ruffles enable non-specific engulfment
86
What is the significance of the green catalytic sites in influenza A’s neuraminidase in Figure 12 and how do they inform antiviral strategies?
Green catalytic sites cleave sialic acid for virion release. Their structure guides inhibitors like oseltamivir
87
How does the 1918 influenza pandemic’s high mortality reflect its zoonotic origins and what are the implications for modern surveillance?
High mortality reflects avian gene reassortment
88
How does the HIV fusion process depicted in Figure 23-20 provide insights into its entry efficiency and what are the limitations of electron microscopy in capturing this process?
Electron micrographs show HIV’s envelope fusing with the plasma membrane
89
What is the role of formins in the trigger mechanism of bacterial invasion and how do they interact with other cytoskeletal elements?
Formins nucleate actin filaments
90
How does the specificity of viral receptors act as a barrier to cross-species transmission and what specific example illustrates this?
Receptor specificity limits viral host range
91
What is the significance of the nicotinic acetylcholine receptor’s role in rabies virus infection and how does it influence the virus’s tissue tropism?
The nicotinic acetylcholine receptor restricts rabies to neurons
92
How does the integration of retroviral DNA into the host genome as described for retroviruses provide a mechanism for latency?
Integration allows retroviruses to remain dormant as proviruses
93
What is the role of the WASP protein in the trigger mechanism of bacterial invasion and how does it interact with the Arp2/3 complex?
WASP activates Arp2/3
94
How does the smallpox virus’s cytoplasmic replication strategy provide an advantage over nuclear-replicating DNA viruses?
Cytoplasmic replication avoids nuclear transport
95
What is the significance of the chemokine receptors CCR5 and CXCR4 in HIV’s evolving tropism and how do their natural ligands influence infection?
CCR5 enables macrophage infection early
96
How does the structure of the influenza C virus’s HEF protein streamline its infection process compared to influenza A?
HEF’s dual role in sialic acid binding and cleavage reduces the need for separate proteins like influenza A’s hemagglutinin and neuraminidase
97
What is the role of the RGD motif in Yersinia’s invasin protein and how does it mimic host cell adhesion processes?
The RGD motif mimics fibronectin’s integrin-binding site
98
How does the trigger mechanism’s use of the SPI1 type III secretion system differ from the zipper mechanism’s reliance on invasion proteins?
SPI1 injects effectors to induce broad cytoskeletal ruffling
99
What is the significance of the actin filament labeling in fluorescence micrographs of Salmonella invasion and how does it confirm the trigger mechanism’s mechanism?
Red-labeled actin filaments surrounding yellow Salmonella in micrographs confirm actin polymerization driven by the trigger mechanism
100
How does the pore-forming strategy of poliovirus differ from the membrane disruption strategy of adenovirus and what are the implications for their respective infections?
Poliovirus forms pores for RNA release
101
What is the role of the sialic acid moiety in the binding sites of influenza A’s hemagglutinin and neuraminidase as shown in Figure 12 and how does it influence antiviral design?
Sialic acid moieties mediate attachment and release. Their structural role in binding sites informs inhibitors like oseltamivir
102
How does the 1957 influenza pandemic’s estimated 116000 US deaths reflect its pathogenicity and what role did avian genes play in its emergence?
The 1957 pandemic’s mortality reflects reassortment with avian genes
103
What is the significance of the electron micrograph in Figure 23-20 for understanding HIV entry and what are its limitations in capturing dynamic processes?
The micrograph shows HIV’s envelope fusion
104
What is the role of formins in the trigger mechanism of bacterial invasion and how do they contribute to its efficiency?
Formins nucleate linear actin filaments
105
What is the significance of the chemokine receptor ligands Rantes Mip1α and Mip1β in blocking HIV infection and how do they inform therapeutic strategies?
These ligands block CCR5
106
How does the influenza C virus’s HEF protein’s dual role in attachment and release provide an evolutionary advantage over influenza A’s separate proteins?
HEF’s combined functions reduce genome size and protein complexity
107
What is the role of the E-cadherin receptor in Listeria’s invasion and how does its specificity influence the bacterium’s tissue tropism?
E-cadherin binding restricts Listeria to epithelial cells
108
How does the SPI1 type III secretion system’s induction of actin-rich ruffles mimic macropinocytosis and what advantages does this provide?
SPI1 effectors induce actin ruffles resembling macropinocytosis
109
What is the significance of the green-colored catalytic sites in Figure 12 and how do they contribute to influenza’s viral release?
Green catalytic sites on neuraminidase cleave sialic acid
110
How does the 2009 H1N2018 H1N1 pandemic’s lower mortality (12500 US deaths) compared to 1918 reflect changes in viral pathogenicity or host factors?
Lower mortality in 2009 reflects milder pathogenicity due to partial immunity from prior H1N1 exposure and improved medical interventions
111
What is the limitation of electron microscopy in capturing the HIV fusion process in Figure 23-20 and how could complementary techniques address this?
Electron microscopy provides static images
112
How does the trigger mechanism’s activation of formins and Rho GTPases contribute to its efficiency in bacterial invasion?
Formins and Rho GTPases synergize to nucleate and stabilize actin filaments
113
What is the role of the Arp2/3 complex in both the zipper and trigger mechanisms and how does its activation differ between the two?
Arp2/3 nucleates actin in both mechanisms. In the zipper mechanism
114
How does the influenza virus’s use of abundant sialic-acid-containing oligosaccharides provide a strategic advantage for its infectivity?
Abundant sialic acid receptors enable influenza to infect diverse cell types
115
What is the significance of the nuclear pore docking strategy of adenovirus and how does it optimize its replication cycle?
Docking at nuclear pores ensures direct DNA delivery to the nucleus
116
How does the integration of retroviral dsDNA into the host genome provide a mechanism for immune evasion?
Integration as a provirus shields retroviruses from immune detection
117
What is the role of the WASP protein in the cytoskeletal dynamics of the trigger mechanism and how does it interact with Rho GTPases?
WASP links Rho GTPase signaling to Arp2/3 activation
118
How does the smallpox virus’s encoding of its own DNA polymerase provide a replication advantage and what are the trade-offs?
Encoding DNA polymerase enables cytoplasmic replication
119
What is the significance of the chemokine receptor CXCR4 in HIV’s late-stage infection and how does its ligand Sdi1 influence viral entry?
CXCR4 enables T-cell infection
120
How does the influenza C virus’s HEF protein’s dual functionality provide an evolutionary advantage over influenza A’s separate proteins?
HEF’s combined attachment and release functions reduce genome size and protein complexity
121
What is the role of the E-cadherin receptor in Listeria’s tissue-specific invasion and how does it influence the bacterium’s pathogenicity?
E-cadherin binding targets epithelial cells
122
How does the SPI1 type III secretion system’s induction of actin-rich ruffles contribute to Salmonella’s broad host cell range and what visual evidence supports this?
SPI1-induced ruffles enable non-specific engulfment
123
What is the significance of the green catalytic sites in influenza A’s neuraminidase in Figure 12 and how do they inform antiviral strategies?
Green catalytic sites cleave sialic acid for virion release. Their structure guides inhibitors like oseltamivir
124
How does the 1918 influenza pandemic’s high mortality reflect its zoonotic origins and what are the implications for modern surveillance?
High mortality reflects avian gene reassortment
125
How does the HIV fusion process depicted in Figure 23-20 provide insights into its entry efficiency and what are the limitations of electron microscopy in capturing this process?
Electron micrographs show HIV’s envelope fusing with the plasma membrane
126
What is the role of formins in the trigger mechanism of bacterial invasion and how do they interact with other cytoskeletal elements?
Formins nucleate actin filaments
127
How does the specificity of viral receptors act as a barrier to cross-species transmission and what specific example illustrates this?
Receptor specificity limits viral host range
128
What is the significance of the nicotinic acetylcholine receptor’s role in rabies virus infection and how does it influence the virus’s tissue tropism?
The nicotinic acetylcholine receptor restricts rabies to neurons
129
How does the integration of retroviral DNA into the host genome as described for retroviruses provide a mechanism for latency?
Integration allows retroviruses to remain dormant as proviruses
130
What is the role of the WASP protein in the trigger mechanism of bacterial invasion and how does it interact with the Arp2/3 complex?
WASP activates Arp2/3
131
How does the smallpox virus’s cytoplasmic replication strategy provide an advantage over nuclear-replicating DNA viruses?
Cytoplasmic replication avoids nuclear transport
132
What is the significance of the chemokine receptors CCR5 and CXCR4 in HIV’s evolving tropism and how do their natural ligands influence infection?
CCR5 enables macrophage infection early
133
How does the structure of the influenza C virus’s HEF protein streamline its infection process compared to influenza A?
HEF’s dual role in sialic acid binding and cleavage reduces the need for separate proteins like influenza A’s hemagglutinin and neuraminidase
134
What is the role of the RGD motif in Yersinia’s invasin protein and how does it mimic host cell adhesion processes?
The RGD motif mimics fibronectin’s integrin-binding site
135
How does the trigger mechanism’s use of the SPI1 type III secretion system differ from the zipper mechanism’s reliance on invasion proteins?
SPI1 injects effectors to induce broad cytoskeletal ruffling
136
What is the significance of the actin filament labeling in fluorescence micrographs of Salmonella invasion and how does it confirm the trigger mechanism’s mechanism?
Red-labeled actin filaments surrounding yellow Salmonella in micrographs confirm actin polymerization driven by the trigger mechanism
137
How does the pore-forming strategy of poliovirus differ from the membrane disruption strategy of adenovirus and what are the implications for their respective infections?
Poliovirus forms pores for RNA release
138
What is the role of the sialic acid moiety in the binding sites of influenza A’s hemagglutinin and neuraminidase as shown in Figure 12 and how does it influence antiviral design?
Sialic acid moieties mediate attachment and release. Their structural role in binding sites informs inhibitors like oseltamivir
139
How does the 1957 influenza pandemic’s estimated 116000 US deaths reflect its pathogenicity and what role did avian genes play in its emergence?
The 1957 pandemic’s mortality reflects reassortment with avian genes
140
What is the significance of the electron micrograph in Figure 23-20 for understanding HIV entry and what are its limitations in capturing dynamic processes?
The micrograph shows HIV’s envelope fusion
141
What is the role of formins in the trigger mechanism of bacterial invasion and how do they contribute to its efficiency?
Formins nucleate linear actin filaments
142
What is the significance of the chemokine receptor ligands Rantes Mip1α and Mip1β in blocking HIV infection and how do they inform therapeutic strategies?
These ligands block CCR5
143
How does the influenza C virus’s HEF protein’s dual role in attachment and release provide an evolutionary advantage over influenza A’s separate proteins?
HEF’s combined functions reduce genome size and protein complexity
144
What is the role of the E-cadherin receptor in Listeria’s invasion and how does its specificity influence the bacterium’s tissue tropism?
E-cadherin binding restricts Listeria to epithelial cells
145
How does the SPI1 type III secretion system’s induction of actin-rich ruffles mimic macropinocytosis and what advantages does this provide?
SPI1 effectors induce actin ruffles resembling macropinocytosis
146
What is the significance of the green-colored catalytic sites in Figure 12 and how do they contribute to influenza’s viral release?
Green catalytic sites on neuraminidase cleave sialic acid
147
How does the 2009 H1N1 pandemic’s lower mortality (12500 US deaths) compared to 1918 reflect changes in viral pathogenicity or host factors?
Lower mortality in 2009 reflects milder pathogenicity due to partial immunity from prior H1N1 exposure and improved medical interventions
148
What is the limitation of electron microscopy in capturing the HIV fusion process in Figure 23-20 and how could complementary techniques address this?
Electron microscopy provides static images
149
How does the trigger mechanism’s activation of formins and Rho GTPases contribute to its efficiency in bacterial invasion?
Formins and Rho GTPases synergize to nucleate and stabilize actin filaments
150
What is the role of the Arp2/3 complex in both the zipper and trigger mechanisms and how does its activation differ between the two?
Arp2/3 nucleates actin in both mechanisms. In the zipper mechanism
151
How does the influenza virus’s use of abundant sialic-acid-containing oligosaccharides provide a strategic advantage for its infectivity?
Abundant sialic acid receptors enable influenza to infect diverse cell types
152
What is the significance of the nuclear pore docking strategy of adenovirus and how does it optimize its replication cycle?
Docking at nuclear pores ensures direct DNA delivery to the nucleus
153
How does the integration of retroviral dsDNA into the host genome provide a mechanism for immune evasion?
Integration as a provirus shields retroviruses from immune detection
154
What is the role of the WASP protein in the cytoskeletal dynamics of the trigger mechanism and how does it interact with Rho GTPases?
WASP links Rho GTPase signaling to Arp2/3 activation
155
How does the smallpox virus’s encoding of its own DNA polymerase provide a replication advantage and what are the trade-offs?
Encoding DNA polymerase enables cytoplasmic replication
156
What is the significance of the chemokine receptor CXCR4 in HIV’s late-stage infection and how does its ligand Sdi1 influence viral entry?
CXCR4 enables T-cell infection
157
How does the influenza C virus’s HEF protein’s dual functionality provide an evolutionary advantage over influenza A’s separate proteins?
HEF’s combined attachment and release functions reduce genome size and protein complexity
158
What is the role of the E-cadherin receptor in Listeria’s tissue-specific invasion and how does it influence the bacterium’s pathogenicity?
E-cadherin binding targets epithelial cells
159
How does the SPI1 type III secretion system’s induction of actin-rich ruffles contribute to Salmonella’s broad host cell range and what visual evidence supports this?
SPI1-induced ruffles enable non-specific engulfment
160
What is the significance of the green catalytic sites in influenza A’s neuraminidase in Figure 12 and how do they inform antiviral strategies?
Green catalytic sites cleave sialic acid for virion release. Their structure guides inhibitors like oseltamivir
161
How does the 1918 influenza pandemic’s high mortality reflect its zoonotic origins and what are the implications for modern surveillance?
High mortality reflects avian gene reassortment
162
How does the HIV fusion process depicted in Figure 23-20 provide insights into its entry efficiency and what are the limitations of electron microscopy in capturing this process?
Electron micrographs show HIV’s envelope fusing with the plasma membrane
163
What is the role of formins in the trigger mechanism of bacterial invasion and how do they interact with other cytoskeletal elements?
Formins nucleate actin filaments
164
How does the specificity of viral receptors act as a barrier to cross-species transmission and what specific example illustrates this?
Receptor specificity limits viral host range
165
What is the significance of the nicotinic acetylcholine receptor’s role in rabies virus infection and how does it influence the virus’s tissue tropism?
The nicotinic acetylcholine receptor restricts rabies to neurons
166
How does the integration of retroviral DNA into the host genome as described for retroviruses provide a mechanism for latency?
Integration allows retroviruses to remain dormant as proviruses
167
What is the role of the WASP protein in the trigger mechanism of bacterial invasion and how does it interact with the Arp2/3 complex?
WASP activates Arp2/3
