Bacteria and Viruses Flashcards
(145 cards)
1
Q
Bacteria are prokaryotes. What are some of the main characteristics of prokaryotes?
A
Prokaryotes have NO nucleus. Specifically, bacteria have a cell well made of peptidoglycan.
2
Q
What are some basic key features of bacterial structure?
A
Smaller than eukaryotes, no nucleus, no organelles, same DNA-RNA-Protein pathway (central dogma), and have a cell well.
3
Q
What are the two different types of bacteria?
A
Gram negative and gram positive bacteria
4
Q
What is a gram-negative bacteria?
A
A bacteria that has a very thin peptidoglycan wall with a complex outer membrane channels. These bacteria also have lipopolysaccharides on the outside of their outer membrane which alters how their interact with the immune system.
5
Q
What is a gram-positive bacteria?
A
A bacteria with a thick peptidoglycan coat surrounding its plasma membrane. The peptidoglycan cell wall is made of peptides and sugars making this type of bacteria more water soluble. Having a thick cell makes bacteria easier to treat as long as they lack resistance.
6
Q
What is the common cause of most urinary tract infections (UTIs)?
A
E. Coli is normally the cause of UTIs. This bacteria resides in the intestines and cause infection when they migrate to the genitourinary tract and begin secreting toxins and lipopolysaccharides.
7
Q
What are some characteristics of E. Coli?
A
E. Coli is a gram-negative bacteria that is rod shaped.
8
Q
What is the minimum inhibitory concentration (MIC)?
A
This is the concentration of a drug that inhibits bacterial growth by 50%.
9
Q
What drug would most commonly be prescribed for a urinary tract infection caused by E. Coli?
A
Nitrofurantoin
10
Q
What are some characteristics about the antibiotic Nitrofurantoin?
A
Broad spectrum antibiotic. Has less resistance to bacteria compared to its counterparts. It is a synthetic drug. Collects in the bladder as well. Bactericidal.
11
Q
What is the MOA of Nitrofurantoin?
A
This drug enters into bacterial cells where it is activated by the bacteria’s nitroreductase. Once activated, this drug damages bacterial DNA, RNA, and ribosomes making the drug bactericidal.
12
Q
What is the difference between a bacteriostatic and bactericidal drug?
A
A bacteriostatic drug stops the bacteria from growing compared to a bactericidal drug that kills the bacteria.
13
Q
What is the difference between a narrow spectrum antibiotic and a broad spectrum antibiotic?
A
Narrow spectrum antibiotics can only affect one type of bacteria while broad spectrum antibiotics can kill several types of bacteria.
14
Q
Why can Nitrofurantoin be used to treat UTIs even though it is a broad spectrum antibiotic?
A
Nitrofurantoin accumulates in the bladder making it a good drug to target urinary tract infections. However, this drug could also hurt some of the good bacteria in the body.
15
Q
What are the pharmacokinetics of Nitrofurantoin?
A
80% of the drug forms a gel in the GIT allowing it to be more readily absorbed and slowly dissolved.
16
Q
What is Acute Bacterial Rhinosinusitis (ABRS)?
A
Inflammation of the sinuses due to bacterial infection.
17
Q
What bacteria is likely the cause of Acute Bacterial Rhinosinusitis (ABRS)?
A
Streptococcus pneumonia. This is a gram-positive bacteria.
18
Q
What antibiotic is typically prescribed in order to treat ABRS?
A
Amoxicillin with or without Clavulanate.
19
Q
What is the MOA of amoxicillin? (Amoxicillin and Penicillin are both Beta-Lactam antibiotics which both work in inhibiting PBP).
A
Amoxicillin competitively inhibits penicillin-binding-proteins (PBP). PBP is a transpeptidase that is responsible for the cross-linking of D-alanine and D-aspartic acid in bacterial cell walls. Without this action of PBP, bacteria are not able to build cell walls leading to bactericidal action.
20
Q
What are the main characteristics of Amoxicillin?
A
Broad spectrum and bacteriocidal drug with a short half-life and low toxicity. Effective against most gram-negative and gram-positive bacteria.
21
Q
Is Amoxicillin effective against non-growing bacteria?
A
No, it is not effective against bacteria not trying to grow their cell wall.
22
Q
What is the significance of different lactam rings inside different variations of the beta-lactam antibiotics?
A
23
Q
What is the deal behind antibiotic resistance regarding production of lactamases by some bacteria?
A
Bacteria have small portions of circular additional DNA called plasmids. These plasmids can produce proteins that break down antibiotics. The plasmid creates beta-lactamases or penicillinases to destroy the beta-lactam ring in beta-lactam antibiotics. these plasmids holding antibiotics resistant data can be shared with other bacteria so they can develop resistance as well.
24
Q
Is there another beta-lactam antibiotic that can inhibit antibiotic resistance?
A
Clavulanate limits bacterial resistance by inhibiting the production of lactamases from bacterial plasmid.
25
What are the main types of antibiotic resistance?
A. Plasmid producing lactamases or penicillinases that break down lactam ring in some lactam antibiotics
B. Altered penicillin binding proteins (PBPs)
C. Decreased permeability to drugs so they cannot reach the PBPs.
26
Penicillin allergies are fairly common. What is the reason for this happening?
Penicillin ends up binding to T cells in the body and activating them which signals an immune response. Typical symptoms include rash, itching, fever, swelling, shortness of breath, and sometimes anaphylaxis.
27
What is the difference between Penicillin and Cephalosporins?
These drug classes inhibit the same target. For mild allergies, Cephalosporins can be used as its chemical structure is slightly different. However, for intense allergies, this drug can not be used.
28
When patients have intense allergies to Penicillin Antibiotics, what is an alternative antibiotic group they could take?
Fluoroquinolones
29
What is the function of the antibiotic group Fluoroquinolones?
Bacteria grows quickly (constant S phase) and, in part, relies heavily on active DNA synthesis. When DNA is replicated, helicases unwind the DNA first, which causes torsional stress. The enzyme called DNA gyrase then goes to unwind or rewind DNA to resolve the torsional stress. Fluoroquinolones inhibit DNA gyrase.
30
What is the specific fluoroquinolone discussed in class?
Moxifloxacin
31
What is the MOA of Moxifloxacin?
Inhibits DNA gyrase, therefore, stopping the replication of DNA. Causes a build-up of broken DNA that the bacteria can not use.
32
What is the bacteria Anaplasma phagocytophilum?
This is a gram-negative bacteria that live inside immune cells called neutrophils. Causes a disease called granulocytic anaplasmosis.
33
How would granulocytic anaplasmosis be treated?
Through the use of the antibiotic group of Tetracyclines. Specifically, the tetracycline antibiotic called Doxycycline.
34
Tetracyclines are approved for children under 8 years old (T/F).
False; Tetracycline antibiotics are NOT approved for children under the age of 8.
35
Why are tetracyclines called what they are called?
Tetracyclines are made up of 4 cyclic rings.
36
What are some basic characteristics of Tetracycline antibiotics?
A bacteriostatic drug that rids the cell of protein. If the drug were to leave the cell, the translation of RNA to protein would begin again. Very hydrophobic drug allowing it a high bioavailability. Very broad spectrum antibiotic.
37
What is the MOA of Tetracyclines?
Bacteria have 2 RNA subunits working when translating RNA to protein. These subunits are the 50s and 30s. These subunits add amino acids to the growing protein chain after they have recruited tRNA to bring the appropriate amino acid. Tetracyclines will actually bind the 30s subunit of RNA, which blocks tRNA and therefore blocks amino acids to build a protein. Therefore, protein synthesis is inhibited.
38
What about the MOA of tetracyclines allows them to act against both gram-negative and gram-positive bacteria?
Protein synthesis within all bacteria is very similar. Since this drug targets the 30s subunit, which all bacteria have, it makes sense that it would not discriminate in the bacteria it stops from producing proteins.
39
What are some things that interfere with the absorption of tetracycline antibiotics?
When taken with dairy products and/or antiacids, tetracyclines are not absorbed as well.
40
What are the adverse effects of tetracycline antibiotic use?
Binds to bone and tooth enamel causing dark discolouration. It can cross the placenta, so it is not used in pregnant women. Can also result in hepatotoxicity.
41
What is another use for tetracyclines discussed in class?
It can be used to treat acne. The bacteria Cutibacterium Acnes goes into pores and causes inflammation. Tetracyclines limit the growth of these facial bacteria by inhibiting their ability to make proteins.
42
Could a TNF inhibitor be used for severe acne?
No! A TNF inhibitor would not allow your body to mount basic immune responses.
43
What is the antibiotic Azithromycin?
This drug targets the 50S subunit of RNA involved in translating RNA to protein. Halts protein production in bacteria.
44
What causes Tuberculosis?
A bacteria called Mycobacterium tuberculosis. This is a gram-positive non-motile rod with a waxy coat around it.
45
What is the typical lifecycle for tuberculosis infection?
This bacteria is breathed in and loves the oxygen-rich environment of the lungs. Once in the lungs, alveolar macrophages phagocytose the bacteria, where they thrive and replicate. With all the immune cells being used to grow the bacteria, a granulosa forms in the lungs. When the structure is left unchecked and ruptured is when the disease is active and spreads.
46
What are the early symptoms of tuberculosis typically from?
Early symptoms are from basic immune responses attempting to defeat the bacteria.
47
What feature of Adalimumab (Humira) would cause a stagnant TB infection to become active?
Adalimumab is a fully human monoclonal antibody that binds TNF-alpha and neutralizes it. This stops the body from being able to mount a proper immune response to an invader, which allows TB to become active and spread throughout the body.
48
How is Tuberculosis treated?
Isoniazid
49
What is the MOA of Isoniazid?
Isoniazid targets mycolic acid synthesis on the waxy layer of the cell wall. This interferes with cell wall synthesis producing a bacteriocidal effect.
50
Drugs without mycolic acid as the outer layer of the cell wall can still be treated with Isoniazid (T/F).
False; Isoniazid only blocks mycolic acid so bacteria without this would NOT be affected.
51
What are some basic characteristics of Isoniazid?
Narrow spectrum antibiotic that is bactericidal.
52
What are DNA viruses?
This is a type of virus that contains DNA as its genetic material and uses DNA-dependent DNA polymerase during replication.
53
What are the different types of DNA viruses discussed in class?
Herpes Viruses (8 different ones; HSV1, HSV2) and Hepatitis B.
54
How does the herpes virus begin its cell cycle?
Infects cells in the nervous system through its outer glycoproteins interacting with receptors on the cell surface. The virus's genetic material will enter the cell, where it then enters the nucleus. Viral circular DNA is transcribed into RNA inside the nucleus of our cells through the use of viral DNA-dependent DNA polymerase. The virus can enter the latent (inactive) or lytic (active) infection stage. This virus can also be reactivated during body stress or immune suppression. Once this infection is in the body, the host will always have it.
55
Which of the following types of nucleic acid synthesis are performed by the virus in this figure?
DNA-to-DNA
56
What drug is used to treat the DNA virus Herpes?
Acyclovir
57
What is the drug Acyclovir?
This drug is a competitive inhibitor for viral DNA polymerase.
58
How does the Km and Vmax change for a competitive inhibitor?
Vmax (Maximum reaction velocity at which all enzymes are saturated with substrate) is unchanged. This makes sense because with enough substrate, you can overcome the competitive inhibition and reach the same reaction velocity.
Km (substrate concentration when half maximum velocity is reached) is increased. This makes sense because you will need more substrate to beat out the inhibitor to reach half the velocity of the reaction.
59
Acyclovir has a Ki for HSV DNA polymerase 0.03 microMoles, human DNA polymerase-alpha 0.15 microMoles and DNA polymerase-beta 11.9 microMoles. Does Acyclovir inhibit human DNA polymerase or HSV DNA polymerase better?
The smaller the Ki, the larger the inhibition would be. This means that Acyclovir inhibits HSV DNA polymerase the best.
60
What is the MOA of Acyclovir?
Prodrug that is taken in the unphosphorylated form via IV. Enters into infected cells, where it is first phosphorylated by viral thymidine kinase. This happens because the drug resembles thymidine. Cellular kinases then add a total of 2 more phosphates for it to be fully active. It enters the nucleus, targets viral DNA polymerase and is incorporated into viral DNA, stopping further replication.
61
What are some basic characteristics of Acyclovir?
Prodrug that is very polar and has poor bioavailability. It only inhibits the virus from replicating and does not kill it. This drug is very safe as well since it is only activated by viral thymidine kinase. Only works well for HSV1 and 2. This is given IV unless an amino acid is added to make it more bioavailable.
62
What can be added to a drug to make it more hydrophilic, nonpolar, and bioavailable?
You can add an amino acid-like valine.
63
Can Acyclovir be given to pregnant women?
Yes. Acyclovir needs the herpes virus to be present to be activated. If there is no infection, then the medication will not work.
64
What is the oral version of Acyclovir?
Valacyclovir is the oral ester version of Acyclovir. It is more bioavailable than acyclovir.
65
Do the drugs we currently have to treat herpes 1 and 2, like Acyclovir and Valacyclovir, actually cure the disease?
No, these medications are NOT a cure. They prevent the virus from replicating.
66
What are the eight different Herpes viruses?
Herpes simplex 1, Herpes simplex 2, Varicella Zoster Virus/ Shingles (VZV), Cytomegalovirus (CMV/HHV5), Epstein-Barr Virus/Mono (EBV/HHV4), HHV6, HHV7, and HHV8.
67
What is Cytomegalovirus (CMV/HHV5)?
Herpes virus that has complications typically for only immune comprised people and newborns. Infects 40-80% of people in the US and remains dormant in the body for life. Easily transmitted through body fluids.
68
What is Vericella Zoster Virus (VZV)?
Herpes virus that causes chickenpox in children and shingles in adults. Often left untreated but can be treated with Acyclovir but only if caught early. PREVENTED VIA VACCINATION.
69
What is Epstein-Barr Virus/ Mononucleosis (EBV/HHV4)?
Herpes virus that is transmitted through saliva. Symptoms include extreme fatigue, fever, and swollen lymph nodes.
70
If someone takes acyclovir and some fraction of the drug ends up in a tissue that is not infected, in what form is the drug?
It would be in its unphosphorylated form.
71
If acyclovir was phosphorylated by a host kinase and not a viral kinase, would it still be safe to use in infants and pregnant women?
No. The only reason this drug is safe is that an active infection activates the drug. If human kinase activated it, it could likely target our own transcription methods.
72
How does HIV begin its life cycle?
HIV binds to proteins on the cell surface of T-cell and endocytosed into the cell. The vesicle breaks down, which releases the RNA capsid for HIV. The RNA is copied into DNA via reverse transcriptase. The new DNA genome enters the nucleus and is incorporated into the human genome. The human/viral DNA is then transcribed into RNA, which is translated into a protein released into the body. Viral proteases will cleave these viral proteins for proper packaging as well. When HIV protein buds off the cell, it is still inactive and must enter circulation and be processed to become active.
73
What are the 4 different ways we currently treat HIV?
1. Integrase strand transfer inhibitor
2. Reverse transcriptase inhibitors (RTIs)
3. Protease Inhibitor
4. Fusion inhibitor
74
What is the drug Abacavir (ABC)?
This is a nucleoside analogue reverse transcriptase inhibitor (RTI).
75
What is the difference between a nucleoside and a nucleotide?
A nucleotide is composed of a phosphate group, a sugar, and a nitrogenous base. A nucleoside contains all of that but not a phosphate group.
76
What is the MOA of reverse transcriptase inhibitors?
RTIs enter the body resembling nucleosides (no phosphate), where they are then phosphorylated three times by host kinase. The drug is then incorporated into a newly forming DNA molecule during reverse transcription. The drug lacks a 3' hydroxyl group, therefore, terminating the DNA chain elongation. It also inhibits HIV reverse transcriptase.
77
What are the two drugs discussed in class that terminate growing DNA chains and are incorporated into them?
Acyclovir and Abacavir
78
How is the pharmacokinetics of RTIs different from that of Acyclovir?
Acyclovir needs an active infection for the drug to be activated however, RTIs have no distinction between infected cells and normal cells as they are phosphorylated by host kinase enzymes.
79
The Nucleoside Reverse Transcriptase Inhibitors (RTIs) are part of a large group of drugs called __________.
AZT
80
Insurance companies price gouged the first medications for AIDS, making sure lower-income areas never received a cure. This resulted in several protests demanding a lower price. These protests also resulted in the discovery of the drug ________________.
Lamivudine (3T3)
81
Nucleosides are __________ into nucleotides.
Phosporylated
82
What are the two Nucleotide Reverse transcriptase inhibitors discussed in class?
Tenofovir (TDF) and Adefovir
83
How does nucleotide reverse transcriptase inhibitors work?
These drugs enter the system already with one phosphate group attached. This ensures it doesn't cross membranes, but we get around this issue by putting additional chemical groups on the phosphate, which allows it to cross membranes. Once at target cell, the drug enters the cell, and extra chemical groups are cleaved off, and the drug is now in active form. It now blocks the HIV reverse transcriptase enzyme stopping the conversion of RNA to DNA. It is also incorporated into viral DNA, causing DNA chain termination.
84
What is PrEP?
This is Pre-Exposure Prophylaxis. It is a combination of emtricitabine and tenofovir called Truvada.
85
There are nucleotide and nucleoside Reverse transcriptase inhibitors. What do the non-nucleotide reverse transcriptase inhibitors (NNRTIs) do?
Non-nucleotide reverse transcriptase inhibitors bind different sites on the reverse transcriptase enzyme than other RTIs. This makes it an allosteric inhibitor that has noncompetitive inhibition.
86
What is a protease?
An enzyme that catalyzes the break down of proteins into smaller polypeptides or amino acids.
87
What are protease inhibitors?
Protease inhibitors target the viral protease that cleaves the HIV-encoded Gag-pol proteins. The uncleaved protein is inactive until it is cleaved. Protease inhibitors bind to proteases and block their activity.
88
What are some strange side effects of protease inhibitors?
Can induce hyperglycemia and abnormal fat distribution.
89
What is always taken with the protease inhibitor, Darunavir?
Taken with P450 protein inhibitors. It is rapidly metabolized by P450 enzymes and must be given with the P450 inhibitor ritonavir, inhibiting the metabolism of Darunavir.
90
What are integrase inhibitors?
Retroviruses start with RNA that must be reverse-transcribed to double-stranded DNA and then integrated into the human genome. The virus uses an enzyme called a viral integrase to incorporate the viral DNA into human DNA. Intergrase inhibitors block the action of this enzyme.
91
What is the intergrase inhibitor discussed during class?
Elvitegravir with the addition of P450 inhibitor, Colbicistat.
92
Steve is a 48-year-old man with a history of HIV. Dating back to the 1980s, he has taken zidovudine and lamivudine, with extensive periods on one or no treatments.
He is currently taking emtricitabine, tenofovir and ritonavir. He has a relatively high viral load and a T-cell count of 50 cells/ul. What options does he have?
For patients at high risk of resistance, the virus can be sequenced, and specific mutations can indicate certain changes in the disease. A fusion inhibitor could now be used to prevent HIV from entering the cell.
93
What are fusion inhibitors?
HIV enters T cells by binding to a viral protein called gp120 and associating with cellular receptor CD4. This association causes a second viral protein called gp41 to undergo conformational change facilitating the cell-virus membrane fusion. Fusion inhibitors bind to gp41 and block the fusion process.
94
What is Hepatitis B and why is is considered strange?
This is a DNA virus. It is a very unusual virus as well. This virus has a unique self-priming mechanism. It brings its DNA into the cell, where it is transcribed into a baby piece of RNA. This RNA is then reverse-transcribed back into single then double-stranded DNA. Hepatitis B is a DNA virus that uses an RNA intermediate and reverse transcriptase enzymes.
95
How is Hepatitis B treated?
Lamivudine and/or tenofovir can be used. Lamivudine would work well because it is a reverse transcriptase inhibitor that blocks the action of RNA being converted to DNA which occurs in the Hepatitis B lifecycle. Tenofovir would also work because it targets the reverse transcriptase inhibitor as well.
96
When would Tenofovir be used to treat Hepatitis B?
Mutations in Hepatitis B polymerase make the virus resistant to lamivudine. Tenofovir seems to have activity against this type of resistant hepatitis B. The efficacy of this drug is measured using liver alanine levels (ALT).
97
What is Hepatitis C?
This is an RNA virus that infects the liver.
98
Describe the Hepatitis C lifecycle in the host cell.
The virus targets the liver as its spike proteins have their receptors in the liver. The virus is then taken up by liver cells, and the RNA genome is released. This RNA is converted to RNA by RNA-dependent RNA polymerase (something we do not do). Some of that RNA is replicated again and packaged into a new viral particle.
99
What type of medication is given to cure Hepatitis C?
Sofosbuvir
100
What is the MOA of the drug Sofosbuvir?
This drug is an inhibitor of the hepatitis C viral NS5B which is the RNA-dependent RNA polymerase. Does not inhibit any host cell's DNA or RNA polymerases. This medication is a cure!
101
What type of medication halts the production of the Hepatitis C virus?
Paritaprevir
102
What is the drug Paritaprevir?
This drug inhibits the HC viral protease called NS3-4A. Normally, this protease cleaves the large viral protein produced to create small active forms. This drug inhibits the action of the protease rendering the virus inactive. Does not cure the Hepatitis C infection.
103
What is a coronavirus?
Coronaviruses are enveloped (lipids on the outer surface) and + strand viruses (RNA converted directly to protein using RNA polymerase). They also have a huge 30 kilobases RNA genome. The genome encodes for a large polyprotein that must be cleaved by viral proteases. Each small piece created can have mutations leading to several different variants.
104
What are the Moderna and Pfizer Covid-19 vaccines made of?
This vaccine is a little piece of covid-19 RNA encapsulated in a stable lipid bubble. This is injected into the arm, where the RNA is translated into protein allowing the body to mount an immune response to the virus.
105
What is the main method of spreading Hepatitis C?
Through injecting drugs with contaminated needles.
106
In 2016, __________ antibiotic prescriptions were written in the US. ________ were thought to be necessary.
270 million; 70%
107
What is the main way of fending off Hepatitis B?
Through the administration of the vaccination for it.
108
What is the J&J Covid-19 vaccination made of?
This is a vaccination with a live adenovirus (one that causes colds). These are not coronaviruses. The virus infects cells and triggers the production of SARS--CoV2 spike proteins allowing an immune response to be mounted.
109
How were scientists originally allowed to work and experiment on covid-19?
There are these cells called Vero E6 African Monkey kidney cells. These cells will happily let viral particles multiply. So this E6 cell will allow for the reproduction of covid-19. Different drugs where then put on these cells to see what would inhibit the growth of the covid-19 virus.
110
How did the drug chloroquine and hydroxychloroquine come into play during the Covid-19 pandemic?
Early reports compared different drugs with their percent inhibition of the covid-19 virus. Early reports did show that chloroquine has some inhibitory action but truly does not work for curing COVID-19.
111
What is the function of the drug Remdesivir?
This drug is used only for hospital-admitted covid-19 patients. It is supposed to overcome to the proofreading activity of the virus, which is made possible by inhibiting the exoN protein. It causes chain termination of the growing viral RNA strand.
112
What does the drug Remdesivir look like?
This drug resembles a nucleotide that has a phosphate with chemical groups attached to mask its charge. Again, this drug causes chain termination by inhibiting RNA-dependent RNA polymerase.
113
What is the drug Paxlovid/ Nirmatrelvir?
This is a protease inhibitor. COVID produces very large proteins that need to be cleaved into smaller active pieces. The protease inhibitor stops the viral protease from cleaving the large protein rendering it inactive.
114
What is the drug Paxlovid/ Nirmatrelvir always given with?
It is always given with a P450 inhibitor. This could be Ritonavir, and it helps to keep protease inhibitor levels high so virus cannot become active.
115
What are some properties of fungi?
These are eukaryotes with a nucleus, organelles, cell walls, and cell membranes.
116
What is Candida Morphogenesis?
This is a dimorphic fungus meaning it can live in the yeast and mold state. This fungus is replicated via budding. Under the right conditions, candida can become invasive and begin to grow filamentous processes.
117
What is the main target of most anti-fungal medications?
Inhibition of ergosterol which is basically fungal cholesterol used in their cell membrane.
118
What are Azole anti-fungal drugs?
The azole anti-fungal class of drugs inhibit lanosterol demethylase, a key enzyme needed in the synthesis of Ergosterol. These drugs inhibit the action of lanosterol demethylase.
119
Human and fungal lanosterol demethylase is similar, and azole drugs inhibit both. What happens to us if our lanosterol methylase is inhibited?
This would also inhibit our bodies from producing sterols which are important for a lot of structural components in the human body.
120
What are the important side effects of azole drugs?
Azole drugs will inhibit human cytochrome P450 proteins with a high enough dose. This can lead to increased concentrations of other drugs metabolized by P450.
121
What is the azole drug discussed in class?
Fluconazole
122
Which of the following is true regarding the influenza virus?
Influenza virus is released from the host cell using a viral-encoded enzyme. (Uses neuraminidase to cleave itself off of host cell membrane)
123
What is the drug fluconazole?
This is the drug of choice for candidiasis fungal infections. It is an azole class drug that inhibits lanosterol demethylase enzyme.
124
What is the MOA of fluconazole?
Fluconazole inhibits the lanosterol demethylase enzyme, which is needed to produce ergosterol, which is needed in the cell membrane.
125
Fluconazole can cross the blood-brain barrier. When would this be useful?
For fungal meningitis.
126
What does the class of anti-fungal drugs called echinocandins do?
These competitively inhibit the synthesis of the fungal cell wall. It is a lipopeptide drug that causes fungal cell walls to lyse.
127
What was the echinocandin drug discussed during class?
Caspofungin
128
Caspofungin is typically used after fluconazole has failed (T/F)
True
129
Why are there limited side effects for the drug caspofungin?
This drug does not act on anything the human body normally contains, so it will not hurt us. Only acts on fungal cell walls.
130
What is the lifecycle of influenza?
This is an RNA virus that begins its replication cycle by binding to a cell surface via the help of hemagglutinin and being endocytosed into the host cell and uncoated. Viral RNA is then converted to RNA by RNA-dependent RNA polymerase. Some viral RNA is translated and released while other ones hang like velcro to the outside of the cell. To be released, though, neuraminidase cleaves the budding viral particle.
131
What are neuraminidase inhibitors?
These are drugs that inhibit the action of neuraminidase, making sure the virus cannot be cleaved off the outside of the cell membrane or disintegrated. This stops the viral infection.
132
What is Tamiflu/ Oseltamivir?
This is a neuraminidase inhibitor. It can only be used when the flu is caught early to stop the spread through the body.
133
What is the drug Baloxavir?
This is an RNA cap-endonuclease inhibitor. The RNA polymerase that influenza produces is a heterotrimer that binds to host RNA. It is then cleaved by the cap-dependent endonuclease (CEN). This new short primer is then used by the viral RNA-directed RNA polymerase to drive viral RNA synthesis. CEN is the target of Baloxavir.
134
Describe how the molecular target of Baloxivir is different from enzymes encoded by the host cell.
The target of Baloxivir is a cap-dependent endonuclease. This is used to help drive RNA synthesis by viral RNA polymerase. Host cells do not contain CEN since we do not convert RNA to RNA.
135
Covid-9 virus is innately resistant to many of the widely used antiviral drugs. Which of the following answers best represents the reason why?
The virus encodes a protein that removes most antiviral drugs from RNA polymers.
136
Refer to the graphs below; which of the following represents the results of the graphs?
Chloroquine has approximately the same activity as Remdesivir for inhibiting the virus.
137
Covid-19 in patients with high levels of inflammation has worse outcomes. THis has opened to door to using anti-inflammatory drugs to treat covid-19 patients. Why is inflammation linked to poor outcomes for covid-19 patients?
Inflammation blocks air exchange in the lungs which is something we are already struggling for with Covid-19.
138
Which of the following statements about HIV replication is true?
Reverse transcriptase inhibitors block the conversion of the HIV genome into DNA.
139
Identify the correct statement about reverse transcriptase inhibitors (RTIs).
Nucleotide RTIs have chemical groups that mask their charge until they enter the cell.
140
Pick the drug class that blocks HIV replication but acts outside the cell after the virus is replicated and released.
Protease Inhibitors
141
Which of the following is a characteristic property of gram-negative organisms?
They bind to a counterstain but not a gram stain. (gram-positive binds both counterstain and gram stain)
142
How does a bacteriostatic drug cause an infection to improve?
Bacteriostatic drugs halt the growth of bacteria but do not kill them. By inhibiting growth, it allows the host immune system to catch up and take out the virus.
143
Which of the following antibiotics inhibits the cross-linking of peptidoglycan polymers in bacteria?
Amoxicillin
144
Which of the following answers best represents the mechanism of action of tetracyclines?
Inhibit translation
145
There is a cure for Herpes 1 and 2 (T/F)
False; this virus hides away in nervous cells and flares up.
