Virals Flashcards

1
Q

What are viruses that live outside of a host cell known as?

A

Virion

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2
Q

What was the first drug known to effectively stop the growth of herpes in immunosuppressed patients

A

Vidarabine or Ara-A

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3
Q

What are the three sub families of herpes virus infection infections?

A

Herpes simplex virus, varicella zoster virus, and cytomegalovirus

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4
Q

Which herpes virus infection can cause Kaposi’s sarcoma

A

HHV-8

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5
Q

What is the viral genome?

A

It is the DNA contents that are ejected to the cell nucleus to use the host machinery and replicate HSV one DNA

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6
Q

What are the signs and symptoms and treatment of HSV –1

A

It is typically asymptomatic, but patients can have oral or Peri oral lesions, ocular infections, non-genital skin lesions, genital skin or mucous membrane lesions and serious, systemic, illnesses, like encephalitis and neonatal disease. It is transmitted from person to person from oral secretions during close contact. The incubation period is one to 26 days and lesions are usually present from one to eight days. It is treated with acyclovir, valacyclovir and famciclovir.

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7
Q

How is the treatment of HSV one determined

A

What are the infection is the first time or a reactivation the severity of the symptoms and what the site of infection is.

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8
Q

What are the nucleotide analogs for HSV infections?

A

Acyclovir, valacyclovir and famciclovir

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9
Q

What are the two clinically significant infections that are caused by varicella zoster?

A

Chickenpox in the primary infection and herpes, zoster and shingles and the reactivation

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10
Q

What is the most common complication of herpes zoster?

A

Posttherapetic neuralgia

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11
Q

How can cytomegalovirus be transferred?

A

It can be bisexual intercourse, close contacts of viral shedding by blood or tissue exposure or vertically through pregnancy or childbirth

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12
Q

What are the nucleotide analogs of cytomegalovirus?

A

Ganciclovir and Valganciclovir

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13
Q

What is the therapeutic goal for treatment of chronic hepatitis b and c

A

Decrease the risk of cirrhosis and hepatocellular carcinoma by suppressing HBV and HCV replication

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14
Q

What are the non-infectious causes of hepatitis?

A

Alcohol and drug exposure, autoimmune disease, or metabolic reasons

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15
Q

How is hepatitis C, most commonly transmitted by?

A

IV drug use unprotected sex with multiple partners surgical exposure, unintended needlestick or sharp exposures hemodialysis HIV and infants of HCV positive mothers.

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16
Q

How soon after infection can you detect hepatitis C on lab work?

A

One to two months after infection

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17
Q

When can you expect chronic liver disease and HCV infection most likely to appear in an infected patient

A

In the third and fourth decades after initial infection

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18
Q

Once the hepatitis C virus enters the body what type of cell does it target?

A

Hepatocytes

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19
Q

What class of oral medication has changed the landscape for HCV treatment so that cure is now possible?

A

Direct acting antivirals

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20
Q

Which virus does amantadine inhibit

A

Influenza A

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21
Q

Which virus is a spherical shape with an external lipid membrane that is taken from a host cell, and a virus multiplies similar to a parasite

A

Influenza virus

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22
Q

What are the steps of the viral replication process

A
  1. Attachment of the virus to a susceptible host sell by uniting with a cell surface receptors
  2. Penetration of the virus or viral genome into the cell and absorbs theenzymes release
  3. The DNA of the phage penetrates through the hole.
  4. The virus replicates.
  5. There’s a release of new infective Verions
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23
Q

What are the two main classes of antiviral drugs used in influenza a and b

A

Neuraminidase inhibitors which are Tamiflu Relenza and rapivab
And Adamantanes or M2 inhibitors which are flumadine and symmetrel

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24
Q

How do the neuraminidase inhibitors treat influenza?

A

They target the NA glycoproteins on the outer lipid layer of the influenza virus

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25
Q
A
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26
Q

How is Zamamivir administered and why?

A

It has poor bio availability, so it must be administered directly into the respiratory tract by inhalation. It is contraindicated in patient to have Poor inhaler technique and patience with H5N1 virus where extra pulmonary virus replication has been detected.

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27
Q

How soon after symptom on set must all neuraminidase inhibitors for influenza be administered to be effective

A

Within 48 hours of symptom onset

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28
Q

Which neuraminidase inhibitor can be administered IV to Childrens, two years and older

A

Peramivir

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29
Q

How do the adamantanes or M2 inhibitors work for influenza treatment?

A

They block the influx of hydrogen ions through M2 proton channel of influenza a and inhibit the un coating and release of free, viral ribbonuclear proteins in the cells cytoplasm

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30
Q

What are the concerns with the use of amantadine and rimantadine for influenza?

A

It can cause dizziness, nervousness, insomnia, and gastrointestinal toxicities

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31
Q

What is a trivalent or quadrivalent influenza recombinant vaccine?

A

A vaccine that’s not prepared with influenza virus or eggs

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32
Q

At what age can children get the influenza vaccine?

A

Six months and older

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33
Q

How soon after administration of the influenza vaccine is it effective?

A

Two weeks

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34
Q

What are the side effects of the inactivated influenza vaccine?

A

Fever, myalgia, mace, and it typically last one to two days

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35
Q

What are the side effects of the live attenuated influenza vaccine?

A

Rhinorrhea, nasal congestion, headache, vomiting, muscle aches, fever, sore throat, and cough

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36
Q

When is the influenza vaccine contraindicated

A

When there is an anaphylactic allergy to chicken eggs or Guillain barre syndrome

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37
Q

What class of antivirals is recommended for treatment of influenza in the United States?

A

Neuraminidase inhibitors

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38
Q

Which class of antivirals is effective only against influenza a

A

Admanatanes

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39
Q

What is the mechanism of action for Oseltamivir?

A

It inhibits the neuraminidase enzyme and reduces viral replication

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40
Q

What is the physical traits of the HIV structure?

A

It is spherical and shape and has a diameter of one 10,000 of a millimeter with an outer coat or viral composed of a lipid by later they have protein copies that produce spikes on the surface of the Verion and each copy consists of a cap made of three molecules called glycoprotein 120 and a stem consisting of three molecules called glycoprotein 41 that anchor of the structure in the viral envelope

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41
Q

What are the seven steps of HIV replication cycle?

A
  1. Fusion of the HIV cell to the host CD4 lymphocyte cell service.
  2. HIVRNA reverse transcript test integration and other viral proteins host CD for sale by a process similar to pinocytosis
  3. Reverse transcript days the enzyme that makes DNA copies of HIVRNA forms viral DNA.
  4. Viral DNA is then transported across the nucleus and integrates into the host DNA.
  5. New viral RNA is used as the genomic RNA or the genetic material carrying all the hereditary information of the new virus to make viral protein
  6. Viral RNA and proteins move to the cell surface and a new immature HIV virus forms.
  7. The virus matures by proteins and enzyme that leaves the longer HIV proteins into individual proteins and then are released into the house bloodstream.
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42
Q

What is the primary HIV infection phase?

A

It is the acute phase of infection of HIV to AIDS

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43
Q

In what phase of HIV infection do 70% of people suffer flu like symptoms

A

The acute primary phase

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44
Q

How long after exposure to the HIV virus does the immune system fight back with killer T cells and B cells

A

2 to 4 weeks after exposure

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45
Q

What is the clinical latency period of HIV?

A

The person infected with HIV may remain free of HIV related symptoms for years, even though HIV continues to replicate and they can still transmit HIV to others.

46
Q

What appears in an HIV patient’s labs after gradual destruction of the immune system?

A

The HIV viral load in the blood dramatically increases and the number of CD4 T cells drops

47
Q

At what point is an HIV infected person diagnosed with AIDS

A

When they have one or more opportunistic infections, like pneumonia or tuberculosis and fewer than 200 CD4T cells

48
Q

What was the first antiretroviral drug?

A

Zidovudine for HIV

49
Q

What is the goal treatment for HIV and AIDS?

A

To extend and improve the quality of life by decreasing viral load to undetectable levels and prevent resistance to antiretroviral drugs and decrease vertical transmission of HIV from a pregnant woman to her child

50
Q

What can you use to prophylactically prevent an HIV infection in the high risk populations

A

Prep has reduce the risk of getting HIV by 74% or you can do topical microbiocides like gels and creams and foams that can be applied in the genitalia prior to sexual intercourse

51
Q

What are the two key types of HIV screening blood tests?

A

HIV antigen – antibody test that can detect HIV 18 to 45 days after exposure or a nucleic acid test that will detect HIVRNA 10 to 33 days after exposure

52
Q

What is the earliest that viral RNA can be detected after an HIV infection?

A

10 days after transmission

53
Q

What should you monitor in patients that are getting antiretroviral therapy?

A

At baseline in every six months, you should do a CBC and CMP a CD4 cell count and correlate it with immune response. You should also assess BUN creatinine and LFT levels.

54
Q

In viral suppression, what do you typically see on labs at about 4 to 8 weeks after treatment is initiated for HIV patients

A

An increase in CD4 counts

55
Q

When is viral load typically checked after starting treatment and what should you expect to see

A

2 to 4 weeks after starting treatment and you should expect to see a significant decrease

56
Q

How often is viral load rechecked in patients with HIV treatment

A

Every one to two months until the level falls below the limit of detection or 50 copies and then it is checked every six months for 2 to 3 years if the patient is stable

57
Q

When should a patient with HIV start therapy?

A

At the time of diagnosis, regardless of their CD4 counts

58
Q

Before starting therapy and HIV positive patients, what should you test for?

A

Genetic mutations that can reverse transcriptase and Proteus genes you should do a genotype HIV drug resistance test

59
Q

In which situations should patients with early HIV infection not delay treatment while waiting on genetic testing

A

In an acute infection or impact pregnant HIV infected women

60
Q

After failed ART for HIV positive patients, what should the following regiment include?

A

Two or three fully active agents

61
Q

What does a person’s initial HIV treatment regimen include

A

Three HIV medication’s from at least two different HIV drug classes

62
Q

What are the reverse transcriptase inhibitor classes for HIV treatment?

A

NRTI and NNRTI and they prevent the HIV enzyme reverse transcriptase converting single-stranded HIVRNA into double-stranded HIVDNA

63
Q

How did the protease inhibitors work for the antiretroviral drugs?

A

They interfere with the HIV enzyme Proteus, which normally cuts or Cleaves long chains of HIV proteins into smaller individual proteins and it stops new viruses from being assembled

64
Q

How does INSTI work in the antiretroviral drug class?

A

It blocks the HIV enzyme integration, which the virus uses to integrate its genetic material into the DNA of the cell it has infected

65
Q

How did the HIV treatment fusion inhibitors work?

A

It interferes with the viruses ability to fuse with cellular membrane prevent preventing HIV from entering the cell

66
Q

How does CR5 antagonist inhibitors work for HIV treatment?

A

It interferes with the viruses ability to bind to receptors on the outer surface of the cell that it tries to enter, and when the binding fails, the HIV cannot affect the cell

67
Q

How did the CD4 attachment inhibitors work for HIV treatment?

A

They block HIV from attaching to CCR5 and CXCR4 co-receptors and entering the cell

68
Q

How do capsid inhibitors work for HIV infection?

A

It interferes with the HIV cap that protects HIV’s genetic material and enzymes needed for replication

69
Q

which treatments are not recommended in the initial treatment of newly diagnosed HIV patients that are treatment naïve

A

Fusion inhibitors CR5 inhibitors and CD4 post attachment inhibitors

70
Q

What can cause resistance in HIV treatment?

A

Genetic drug resistance, previous exposure to prep

71
Q

How is failure of antiretroviral therapy defined

A

Sub optimal, viral suppression or loss of suppression or inability to maintain appropriate CD for cell count or clinical disease progression

72
Q

What are the possible reasons for ART regimen failure

A

No adherence, drug toxicity, drug drug interactions, development of resistance, etc.

73
Q

What is the basic strategy for treatment failure due to suspected resistance in ART

A

Choose a new regimen, including at least two new drugs, but three is preferred and test for genetic drug resistance

74
Q

What is the most common given NRTI for HIV treatment?

A

Lamivudine (epivir or 3TC)

75
Q

What are the common adverse effects of lamivudine

A

Headache, malaise, fatigue, nausea, vomiting, diarrhea, abdominal pain, cough, and nasal congestion, and rarely could cause pancreatitis, aplastic anemia, and lactic acidosis

76
Q

What is the most common NNRTI given for HIV

A

Efavirenz (sustiva)

77
Q

What are the adverse effects of efavirenz

A

Rash liver toxicity, CNS effects fetal malformation and it can interact with many CYP450 drugs

78
Q

What pregnancy category is efavirenz

A

Pregnancy category D and it showed teratogenic effects in animals

79
Q

How does NNRTI affect other HIVART drugs?

A

It increases the metabolism of the
ARTs

80
Q

What is the most common HIV protease inhibitor

A

Ritonavir or norvir

81
Q

What are the adverse effects ritonavir

A

GIF effect endocrine and metabolic effects hepatotoxicity neuromuscular and skeletal effects and CNS effects.

82
Q

What does ritonavir interact with?

A

CYP 450 substrate inhibitors and inducer and it enhances or boosts the efficacy of other HIV drugs

83
Q

What is the most common HIV integrate strand inhibitor?

A

Raltegravir or isentress

84
Q

What are the adverse effects of raltegravir

A

CNS effects, metabolic and endocrine effects, G.I. and hepatic effects and hematologic effects

85
Q

How does raltegravir affect PPI and statin drugs?

A

It increases an enhances their effects

86
Q

What is the most common fusion inhibitor for HIV treatment?

A

Enfuvirtide or fuzeon

87
Q

What are the adverse effects of enfuvirtide

A

Injection site reactions GI effects, fatigue and pneumonia

88
Q

Which HIV drug increases the risk for bacterial pneumonia

A

The fusion inhibitor enfurvirtide

89
Q

What drug increases the concentration of protease inhibitors

A

Fusion inhibitors like enfurvirtide

90
Q

What is the most common CCR5 antagonist?

A

Maraviroc or selzentry

91
Q

What are the adverse effects of CCR5 antagonist?

A

Cough, upper respiratory infection, rash, liver injury, cardiovascular events like postural hypotension, and CNS effect.

92
Q

What drugs should you monitor carefully when giving a CCR5 antagonist

A

Any CYP3A4 isoenzymes

93
Q

What is the most common CD4 for attachment inhibitor

A

FOSTEMSAVIR or rukobia

94
Q

What are CD 4 attachment inhibitors used in

A

Treatment and experienced patients with multi drug resistant, HIV and limited treatment options

95
Q

What are the adverse effects of the CD four attachment inhibitor fostemsavir

A

Hepatotoxicity and QT prolongation

96
Q

What drugs does fostemsavir interact with?

A

Drugs metabolized by CYP3A

97
Q

What is the most common capsid inhibitor?

A

Lenacapavir or sunlenca

98
Q

What are the adverse effects of the capsid inhibitor?

A

Nausea and injection site reactions

99
Q

What drugs should you avoid with capsid inhibitors?

A

Strong and moderate CYP3 a inducer digoxin anticonvulsants and statins

100
Q

Which two of the ART drug classes are not recommended to treat naïve patients

A

Fusion inhibitors and CCR5 antagonist

101
Q

Can patients taking ART for HIV take holidays from their daily drug regimen and how do you advise?

A

No, they cannot take holidays and stopping therapy can lead to a decrease in CD4 cell counts and increase HIVRNA

102
Q

What is the earliest possible time that primary HIV can be detected and what type of test can be used?

A

The earliest is 10 to 33 days after exposure and a NAT test must be used

103
Q

How do viruses replicate?

A

They attach and penetrate the host cell and then use the host cell to produce multiple copies of their genome, then assemble the genetic material into packets and finally create new viruses that are released from the host cell

104
Q

How is the risk for viral transmission among humans determined

A

By characteristics of the virus and the host population

105
Q

What is the treatment options for HSV 1?

A

Acyclovir for 5-10 days within 72 hours of symptom onset or topical acyclovir.

106
Q

Which class of HAART has the least drug interactions?

A

NRTI lamivudine

107
Q

Which class of HAART is pregnancy category D and should only be given if absolutely necessary in pregnancy

A

NNRTI efavirenz

108
Q

Which class of HAART causes insulin resistance?

A

Protease inhibitors like ritonavir

109
Q

Which three classes of HAART are nog recommended in 1st line treatment

A

FI, CCR5 antagonist and CD4 post attachment inhibitor