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Unit 2 > Micro/Immuno > Flashcards

Micro/Immuno Flashcards

1
Q

host-parasite relationship in humans

A

dynamic; based on the immune system of the host and the virulence factors of the parasite

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2
Q

most common parasitic diseases in the US

A
  1. Trichomoniasis: (Tricomonas vaginalis) sexually transmitted
  2. Giardiasis: (Giardia lamblia) loss of appetite and diarrhea
  3. Cryptosporidiosis: (Cryptosporidium) from bad water and causes diarrhea
  4. Toxoplasmosis: (Toxoplasma gondii) raw meats and congenital transmission in cats
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3
Q

parasite lifecycles

A

immature parasite partially develops in an intermediate host then grows to maturity in a principal/definitive host

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4
Q

the 2 classifications of parasites

A
  1. Parasitic Protozoa (Unicellular)

2. Parasitic Helminths (Multicellular) –> “-todes”

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5
Q

5 ways host animals can be infected by parasites

A
  1. ingestion of larvae, eggs or cysts
  2. eating the intermediate host
  3. penetration of parasite into host (foot–>vessels–>heart–>lungs–>ingested–>SI)
  4. maternal transmission (congenital)
  5. vector transmission
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6
Q

parasitic diseases

A

can be gastrointestinal, blood borne or in tissues, chronic but may remain dormant until host is immunosuppressed and may not show symptoms or could be life threatening

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7
Q

innate immune system

A

prevents colonization through release of specific immune cells and cytokines

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8
Q

adaptive immune system

A

antibody formation to damage, neutralize and prevent spread of infection

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9
Q

eosinophilia

A

high WBC count; eosinophils can destroy parasites

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10
Q

IgE

A

increases with parasitic infections and binds to mast cells and basophils; binds to antigen and its Fc portion binds to cells inducing degranulation

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11
Q

the 6 defense mechanisms of parasites from protective host responses

A

antigenic:

  1. concealment (antigens in host’s cells)
  2. variation (novel antigens by mutation)
  3. shedding
  4. mimicry (incorporation of host antigens on parasite’s surface)
  5. immunological subversion
  6. immunologic diversion (polyclonal B-cell activation)
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12
Q

bacteria vs. parasites

A

bacteria have simple lifecycles and are unicellular whereas parasites have complex lifecycles and can be either unicellular (protozoa) or multicellular (helminthes)

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13
Q

obligatory parasite

A

dependent on host

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14
Q

facultative parasite

A

free-living in the environment or parasitic

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15
Q

accidental parasite

A

affects unusual host

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16
Q

temporary parasite

A

visits host for feeding

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17
Q

permanent parasite

A

lives in (endoparasite) or on host (ectoparasite)

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18
Q

opportunistic parasite

A

produces disease in an immunodeficient host

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19
Q

Creutzfeldt-Jacob disease

A

most frequent of the human prion diseases

three different types: (Sporatic-sCJD, Familial- fCJD and Iatrogenic- iCJD)

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20
Q

sCJD symptoms

A

spongiform encephalopathy, rapid loss of brain function (concentration, memory and judgment difficulties), mood changes, sleep disturbances, myoclonus provoked by startle and death within one year (1/1,000,000 have it)

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21
Q

cause of prion diseases

A

proteins (protein-only hypothesis); differences in prions lead to incubation differences

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22
Q

how to sterilize prions

A

autoclaving since they are resistant to conventional physical decontamination methods

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23
Q

vCJD symptoms

A

loss of brain function (slower than sCJD), peripheral pathogenesis involving lymphoreticular tissues, death

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24
Q

Variant Creutzfeldt-Jacob disease

A

type 4 prion (detected by ring of spongiform vacuoles after staining), bovine-to-human transmission of BSE (not in muscle or milk), 1/2,000 carry it and incubation period is 20-30 years

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25
Q

sCJD diagnosis

A

brain biopsy, detection of 14-3-3 protein in CSF, EEG pattern or abnormal T2-weighted MRI signal

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26
Q

PrP^c

A

35 kDa glycoprotein encoded by Prnp gene in host

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27
Q

PrP^sc

A

Scrapie/misfolded form of PrP^c that leads to prion disease and comes from a mutation of exogenous source
*there are 4 types distinguished by bands produced from protease digestion by proteinase K

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28
Q

prion self replication mechanism

A

native and prion conformers bind creating the “seed” which increases in size to an amyloid fibre (aggregates of insoluble fibers) which disseminates by fragmentation to spread the infection

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29
Q

populations infected with sCJD vs. vCJD

A
  • sCJD- mean is 65 years old with a higher prevalence slightly in females and significantly in whites
  • vCJD- mean is 29 years old
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30
Q

BSE and vCJD patterns

A

BSE peaked in 1992 whereas vCJD peaked 8 years later in 2000 due to BSE’s predicted incubation period os 10-20 years

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31
Q

viruses are referred to as:

A

“filterable agents” since they are so small that they pass through a filter (pores= 220nm)

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32
Q

virus replication

A

they only replicate in cells thus are obligate intracellular parasites (do not form colonies on agar plates such as bacteria)

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33
Q

virus diversity

A

very genetically variable and there are many virus species

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34
Q

caspid

A

protein shell that encapsulates the nucleic acid genome and can be helical or icosahedral (20-sided crystal) in symmetry

**capsid shape is independent of genome

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35
Q

virion

A

the particle encoded by a virus genome which can be enveloped (lipid bilayer coating obtained from host cell) or naked (lacking an envelope)

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36
Q

3 basic gene modules of viruses

A
  1. capsid proteins
  2. replicon (has what is necessary for replication)
  3. proteins (interact with the host)
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37
Q

virus classification

A
  1. Host Cell/Kingdom
    - eukaryotic or prokaryotic
    - plant, insect or animal
  2. Genome Type
    - RNA or DNA
    - single or double stranded
  3. Virion Structure
    - enveloped or naked
    - helical, icosahedral or complex
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38
Q

survival mechanisms of viruses

A
  1. capsid for protection (is encoded by genome)
  2. information in genome to help with infection, replication, intracellular survival and virion assembly
  3. transmission to a new host ensures that the virus will not die off
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39
Q

nucleocapsid

A

at the center and similar to the caspid

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40
Q

tegument

A

gel that is in between capsid and envelope

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41
Q

matrix

A

gives structure that lies underneath the envelope

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42
Q

envelope

A

membrane surrounding the particles (lipid bilayer contributed by the host cell)

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43
Q

glycoproteins vs. spikes

A

spikes embedded in the membrane which require glycosylation whereas spikes or fibers do not require glycosylation

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44
Q

inside to outside structure of virus

A

genome–>nucleocapsid–>tegument–>matrix–>envelope–>glycoprotein–>spikes

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45
Q

cytopathic effects (CPE)

A

damage to host cells that can be brought on by virus infection that can be used to study virus replication and infectivity

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46
Q

what does a virus need for growth?

A

the right host (tropism), correct receptors (susceptible), appropriate intracellular environment (permissive), biosynthetic machinery (virus does not have genes for this so the healthy cell’s machinery is used), building blocks (nucleotides, ATP, lipids, sugars and AA’s)

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47
Q

steps of virus replication

A
  1. recognition
  2. attachment
  3. entry (penetration of fusion)
  4. uncoating
  5. mRNA transcription
  6. protein synthesis (translation)
  7. replication of genome
  8. virions assembly
  9. egress (lysis, budding or exocytosis)
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48
Q

host range

A

the preferred species

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49
Q

tissue tropism

A

the preferred cell type/host

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50
Q

susceptible

A

cells that a virus can enter due to their receptors

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51
Q

permissive

A

an appropriate intracellular environment allowing for virus replication and virion synthesis

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52
Q

penetration

A

engulfment of entire virion into cell through receptor-mediated endocytosis, phagocytosis or pinocytosis

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53
Q

fusion

A

envelope of virion fuses with the plasma membrane leaving parts of the virion behind

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54
Q

eclipse phase

A

starts with the uncoating of the caspids to release the genome into the cytoplasm of the host cell

no virus is recovered during the replication and assembly phases

ends with the assembly of virions in which viral DNA is inserted into capsid proteins that have formed an empty shell

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55
Q

where can uncoating occur?

A

the plasma membrane, within endosomes and at the nuclear pore

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56
Q

what regulates mRNA synthesis?

A

viral and host transcription factors

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57
Q

what makes mRNA?

A

viral or host polymerases

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58
Q

what translates the viral mRNAs?

A

the host machinery translated them into protein

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59
Q

how is the genome replicated?

A

viral and host DNA and RNA polymerases make new genomes using host cell nucleotides

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60
Q

routes of transfer of cell associated virions

A

cell-to-cell spread and cell fusion (syncytium formation)

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61
Q

this produces virus plaques

A

cell lysis

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62
Q

RNA viruses

A

RNA is the genetic material and the template for protein synthesis

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63
Q

RDRP

A

RNA-Dependent RNA polymerase, located in the cytoplasm, efficiently transcribes RNA into mRNA and helps copy the genomes of RNA viruses on cell membranes

  • used since cells do not have enzymes to do this
  • low fidelity
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64
Q

sense strand

A

+ strand of mRNA

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65
Q

antisense strand

A
  • strand the is the template for mRNA
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66
Q

Poliovirus (Picornaviridae)

A

+ ssRNA genome with linear mRNA molecule which recognizes CD155 receptor and infects epithelial cells only in humans but can spread to muscles and neurons

can be prevented with vaccination with a live or killed virus and its transmission is fecal-oral and persists in water supply

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67
Q

Poliovirus entry

A

conformational change is induced once bound to receptor

capsid proteins become hydrophobic and RNA genome enters at plasma or endosome membrane

68
Q

Rotavirus disease

A

causes severe gastroenteritis especially in children leading to dehydration which can be treated by oral rehydration solutions and prevented by live-attenuated vaccines

has segmented genome and once virions are assembles, they bud into the RER

69
Q

influenza virus disease

A

acute respiratory illness in two types: uncomplicated and complicated

  • ssRNA with segmented genome which is trafficked to the nucleus for transcription and replication by RDRP

virions assemble and egress by budding

there is an accumulation of viral proteins and genome segments at the plasma membrane

70
Q

HIV cell tropism

A

virus binds to CD4 and chemokine receptors on T cells and macrophages

71
Q

stages of HIV disease

A
  1. transmission
  2. acute phase (primary HIV infection)
  3. seroconversion (production of antibodies)
  4. latent period
  5. early symptomatic HIV infection
  6. AIDS- CD4 below 200
  7. advanced HIV infection- CD4 below 50
72
Q

differences in replication in DNA viruses

A

host RNA polymerase- transcription of mRNA

host or viral DNA polymerase- replication of the genome

73
Q

viral TF’s

A

virulence factors

74
Q

DNA polymerases vs RDRP

A

higher fidelity and DNA viruses are generally more stable

75
Q

adenovirus disease

A

pharyngoconjunctival fever, bad cold

transmission: aerosol, fecal-oral

stressed individuals and children are susceptible populations

host RNA pol II- mRNA
viral DNA pol- genome

treatment= cidofovir but can be prevented by vaccination

76
Q

human papilloma virus diseases

A

most commonly diagnosed sexually transmitted infection
warts (treated by excision), or malignancies (treated by oncotherapy)

Gardasil and cervarix are vaccines

tropism- differentiated epithelial cells

77
Q

HIV drugs

A

NRTI (nucleoside reverse transcriptase inhibitors)
NNRTI (non-nucleoside reverse transcriptase inhibitors)
PI (protease inhibitors)
INSTI (integrase strand transfer inhibitors)
CCr5 antagonists

78
Q

ART

A

antiretroviral therapy which combines drugs to avoid resistance

79
Q

HIV lifecycle

A

FILL THIS ONE IN - 179 in notes

80
Q

Herpesvirus

A

8 varieties which cause infections only in humans

81
Q

HV life cycle

A

each HV targets a specific cell type inserting DNA genome into nucleus for mRNA transcription and genome replication (by viral polymerase); egress by exocytosis

82
Q

HV latency

A

genome is present but infectious virions are absent (barrier to vaccines)

83
Q

primary vs. recurrent

A

primary infection can happen from exposure and transmission in children or after asymptomatic shedding during latency or recurrent disease in adults

84
Q

asymptomatic shedding

A

production of virions without even knowing it

85
Q

HSV-1

A

Primary- close contact producing lesions and gingivostomatitis; latency established in neurons

Recurrent- tingling with contagious lesions

86
Q

KSHV (HHV8)

A

Kaposi Sarcoma Herpes Virus
high prevalence in Africa and Mediterranean causing infection of B cells and endothelial cells and malignancies on those immunosuppressed (lesions)

no treamtments

87
Q

final thoughts about HV

A

infections last a lifetime but usually do not cause an issue
asymptomatic shedding is the norm

immunosuppression is a risk for HVs to reactivate
antiviral therapy is helpful

88
Q

Roseola infantum

A

HHV6b and HHV7 infecting CD4+ T cells characterized by a 3 day high fever and faint rash transmitted in saliva

diagnosis- rule out allergy
no treatment but avoid antibiotics
no prevention but maintain normal hygiene

89
Q

Primary VZV

A

varicella (chicken pox)
aerosol transmission which is highly contagious and produces a rash
latency in dorsal root ganglia neurons
could lead to complications

90
Q

Recurrent VZV

A

Herpes Zoster (Shingles)
common in the elderly and immunocompromised
prodrome and contagious lesions
severe complications can occur

91
Q

HSV-2

A

Primary- from close contact between mucous membranes and acquired in adulthood causing lesions below the waist

Recurrent- prodrome and contagious lesions but shedding and transmission can occur without symptoms

92
Q

HSV in the brain

A

Primary could cause meningitis while recurrent could cause encephalitis

HSV targets temporal lobe

93
Q

HSV diagnosis and treatment

A

serology or PCR to distinguish between HSV-1 and HSV-2 while Acyclovir is the parent drug

no vaccines but prevent with safe sex, avoiding cold sore contact and Valtrex or Famvir for daily use to prevent outbreaks

94
Q

VZV diagnosis and treatment

A

can be prevented with vaccines (live attenuated viruses)
diagnosis- clinical signs, PCR and serology
treatment- Zoster for first 3 days

95
Q

Epstein Barr Disease

A

infection of oral epithelial cells and B cells transmitted by saliva which can reoccur during immunosuppression from EBV in B cells

malignancy- lymphoma
diagnosis- clinical signs, serology and blood smear for elevated WBC

96
Q

Cytomegalovirus

A

usually asymptomatic but mononucleosis symptoms could occur
congenital transmission is high and could lead to hearing loss but can be treated by antiviral drugs

affects AIDS patients and transplant recipients

97
Q

characteristics of viral genomes

A 
DNA or RNA
single or double stranded
linear or circular
one segment or multiple segments
single copy of each gene
2-200 genes (not enough for independent survival)
98
Q

what 2 components make up a viral gene

A
  1. enhancer/promoter region
  2. ribosomal entry site
  3. open reading frame

**eukaryotic without operons and expression is induced by binding cellular transcription factors to promoter regions

99
Q

2 differences between bacteria and viruses

A

bacteria- have operons and expression is induced by the interaction of the operator and the repressor/inducer

viruses- no operons and expression is induced when cellular transcription factors bind to promoter regions

100
Q

simple genome

A

genes are in a linear arrangement on one RNA strand and there is only one promoter

101
Q

complex genome

A

genes are on both strands to DNA and can overlap with each having a promoter

102
Q

proteases

A

cleave polyproteins and are essential for drug targets

103
Q

how are viral genomes efficient?

A
  1. no non-coding regions to save space
  2. overlapping reading frames
  3. translational frameshifts
  4. splicing changes AA sequence
  5. polyproteins
104
Q

stability of DNA and RNA viruses

A

RNA- unstable causing one mutation per generation

DNA- stable causing one mutation per several hundred or several thousand generations

105
Q

gene therapy

A

the transfer of appropriate genes to a patient in order to correct or prevent disease

*delivery of gene therapy by viruses involves host-range mutants

106
Q

problems associated with gene therapy

A

short duration of expression and low efficiency of gene transfer

107
Q

problems with the use of viruses for gene therapy

A

severe inflammation and the insertion of viruses into a recipient’s genome could lead to malignany disease

108
Q

complementation

A

two defective viruses that cannot grow independently but can grow when combined since they make up for what each other lacks

109
Q

phenotypic mixing

A

the exchange of capsid proteins between healthy viruses. this produces viruses with phenotypic mixtures which cannot replicate

110
Q

recombination

A

similar genomes will cross over after they overlap at regions of homology thus causing the production of new/hybrid viruses

111
Q

interference

A

infection by one viruses tends to prevent infection by another (blocking receptors and competing for resources)

112
Q

pseudotype

A

the genetic material of one virus in the capsid or envelope of another

113
Q

where do we encounter viruses?

A

people, animals, food, water, insects

114
Q

mechanisms of viral transmission

A
  1. respiratory
  2. fecal-oral
  3. contact
  4. zoonoses
  5. blood
  6. sexual
  7. maternal-neonatal
  8. genetic
115
Q

what does the susceptibility and severity of viral diseases depend on?

A

nature of exposure
viral dose
status of person
virus-host interactions

116
Q

smallpox

A

acquired through respiratory tract
disseminates in the blood
sheds from pustules on the skin

117
Q

virus entry into GI

A

M cells sample the gut contents which includes the virus and presents it to underlying immune cells
**viruses infect M cells and therefore can reach the blood stream

118
Q

IgA

A

offers protection and is present in the gut lumen (immunity to infection)

119
Q

route of pathogenesis of viruses

A

surface of body–> lymph nodes and blood stream–> primary viremia –> secondary viremia–> transmission

120
Q

primary viremia

A

leads to replication in internal organs which may occur without symptoms (incubation stage)

121
Q

secondary viremia

A

disseminates the virus to organs where it is shed

122
Q

chicken pox

A

transmitted by respiratory route affecting epithelial cells and fibroblasts which is spread by viremia to the skin

  • *latent infection = in neurons
  • *reactivation by immune suppression
123
Q

excretion of HIV-1

A

in blood plasma, lymphocytes, CSF (as measured by PCR)

124
Q

severity of virus

A

may be unnoticed, cause illness, induce autoimmunity, be persistent, or be lethal

125
Q

what does it mean to be a successful virus

A

avoids destruction by the immune system and avoids destroying the host before replication is finished so it can be transmitted to others and live even if the host dies

126
Q

general patterns of infection

A 
acute
persistent
latent
slow
transforming
127
Q

why are symptoms caused

A

they are the response of the host to the infection by the virus

128
Q

what causes cell injury

A

a combination of virus replication and the host response

129
Q

Norwalk virus

A

+ssRNA that is transmitted fecal-orally from contaminated water and food

resistant to usual means of disinfection
treatment- hydration
symptoms- diarrhea, vomiting, cramps, fever, malaise

prevention- hand washing, sanitation

130
Q

direct effects

A

cell lysis

cell inactivation

131
Q

indirect effects

A

immunopathology (host immune response to a virus may be the sole cause of disease)

132
Q

HOST factors that contribute to a viral infection

A 
immune status
route of exposure
age
habits
barriers to dissemination
contagiousness
133
Q

VIRUS factors that contribute to a viral infection

A 
antigenic diversity
infectious dose
cell killing/inactivation
pattern of infection
ability to disseminate
shedding
134
Q

how are hepatitis viruses related?

A

they are NOT closely evolutionary related to each other

*symptoms are similar because they all infect hepatocytes

135
Q

how are the hepatitis viruses transmitted?

A

A- fecal-oral

B/C- sex/blood/birth

136
Q

which of the hepatitis viruses can be vaccinated against?

A

A and B

137
Q

diagnosis by serology for Hep A, B and C

A

A- IgM- acute; IgG- recovered/vaccinated

B- viral surface antigen- acute; IgG against viral surface antigen= recovered/vaccinated

C- EIA (real or false positive), RIBA= confirmation

138
Q

when should alternative medicine be used?

A

in addition to prescribed treatments for chronic Hep B and C when there is uncertain prognosis and treatment is grueling

139
Q

Hep B and C treatment

A

polymerase inhibitors +IFN (has many side effects and are often ineffective)

first-generation protease inhibitors are improving treatment of serotype 1 (but have their own side effects)

second generation antiviral released last winter are producing exciting early results

140
Q

Acyclovir

A

for Herpesvirus

nucleoside analog of guanosine

derivatives= valtex (valaciclovir), denavir (penciclovir), famvir (famciclovir)

141
Q

Ganciclovir

A

for CMV

toxic

nucleoside analog of guanosine

derivative= Valcyte

142
Q

Broadspectrum antiviral drugs

A

Foscarnet
Cidofovir
Ribavirin

143
Q

Foscarnet

A

inhibits viral DNA polymerase

IV

damage to kidneys

144
Q

Cidofovir

A

nucleoside analog to cytosine

Herpesvirus, Adenovirus, Papillomavirus, Poxvirus

145
Q

Ribavirin

A

nucleoside analog of guanoside

off-label use

Hep C

146
Q

Drugs for Hep B

A

drugs for Hep C or HIV

Entecavir
Tenofovir

147
Q

Drugs for Hep C

A

combination therapy- peg-interferon-alpha with Ribavirin

sofobuvir combined with peg-interferon-alpha and ribavirin

sofobuvir combined with NS5A inhibitors (Daclatasvir or Ledipasir)

148
Q

NS5A inhibitors

A

Baclatasvir or Ledipasir

*combine with Sofobuvir to treat HepC

149
Q

AZT

A

drug for AIDS

nucleoside analog of thymidine

NRTI

150
Q

Sofosbuvir

A

nucleoside analog of uridine

inhibits RDRP

chain terminator

151
Q

Drugs for influenza

A

Tamiflu (Oseltamivir)
Relenza (Zanamivir)

**sialic acid analogs that inhibit salidase

***virions remain attached to cell

152
Q

unique things about fungi

A

no peptidoglycan
no 70S ribosomes
eukaryotic heterotrophs
grow in cold, dry, high pressure environments

153
Q

yeast

A

single celled
reproduce by budding
closed fungal mitosis

154
Q

mold

A

complex reproduction
grow in hyphae/mycelia
fungal mitosis

155
Q

conida

A

asexual spores

  1. Arthrospores- fragmentation at end of hyphae
  2. Blastospores- from budding
  3. Conidospores- chains at ends of hyphae
  4. Chlmydospores- resistant, round, thick-walled
  5. Sporangiospores- in sac
156
Q

antifungal agents

A
  1. Polyenes- toxic, effective, disrupt membranes where ergosterol binds; Amphotericin B
  2. Azoles- less toxic, prevent ergosterol synthesis; Fluconazole and Diflucan treat candidiasis and cryptococcosis
  3. Echinocandins- low toxicity, prevent beta-glucan synthesis; effective against candida and aspergillus
157
Q

how to diagnose fungi

A 
PPD
KOH-mount microscopy with fungal stains
culture on Sabouraud's agar
PCR- dangerous systemics
Serology- epidemiology
158
Q

superficial mycoses

A

fungal growth on superficial skin layer
thermal dimorphism is NOT required
common but symptoms are minor
treat with topical azoles and oral griseofulvin

example: dermatophytosis

159
Q

dermatophytosis

A

type of superficial mycoses

infects superficial keratinized structures
produces keratinases
symptoms- tinea (jock itch, ringworm, athletes foot)
transmission by fomites and autoinoculation
treat with topical azoles or oral griseofulvin

160
Q

subcutaneous mycoses

A

introduced by trauma
slow spread to trunk by lymphatics
thermal dimorphism
history of ineffective antibiotic treatment
treatment–> oral azoles and Amphotericin B (polyene)

example- sporotrichosis

161
Q

Sporotrichosis

A

type of subcutaneous mycoses

painless ulcer- spreads up lymphatics
diagnose by biopsy and culture (pus)
treatment- oral azoles and Amphotericin B

**complications:
pulmonary (if COPD present)
meningitis (if immunosuppressed)

162
Q

systemic mycoses

A 
environmental-spores in soil
inhaled into lungs
thermal dimorphism
range of severity (clearance--> death)
NOT transmitted person-to-person
mimics TB

example- coccidioides

163
Q

coccidioides

A

systemic mycoses

US southwest
thermal dimorphism
mold in wet then arthrospore release in dry
risk factors- age, pregnancy, race, immunocompromised
diagnosis- exam, PPD, history, biopsy, culture, serology
treatment- oral azoles, Fluconazole, Amphotericin B

***mild (asymptomatic/flu), moderate (valley fever), and severe (pneumonia)

164
Q

opportunistic mycoses

A

varied disease/severity based on host’s pre-existing conditions
optimal treatment- treat infection and underlying problem

example: cryptococcosis

165
Q

cryptococcosis

A

opportunistic mycoses

environmental
suppressed inflammatory response
meningitis, skin nodules, pulmonary issues
diagnosis- biopsy
treatment- oral azoles and Amphotericin B

166
Q

Stribild

A

4 drug combination for HIV

  • includes Cobicistat (prevents liver from breaking down drugs)
  • AZT (Zidovudine) is also used for HIV
167
Q

Cobicistat

A

one of the components of Stribild that prevents the liver from breaking down drugs (it is a liver enzyme)

Unit 2 (3 decks)

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