D.

Antimisiaris 2015
Antivirals Study Guide

Antiviral Agents
Explanation of Objectives:
These are very general objectives to help you understand the thought process of
antiviral medication management.
For the purposes of the exam, the practice questions represent the topics and
format of questions you will see. The practice questions focus on general
mechanisms of how antiviral agents work, adverse drug events (reactions) per drug,
or class of drugs that are notable, and highlights of clinical uses.
Dr. Ds understanding is that for Step 1, the knowledge is much less detailed than
our soft chalk, focusing on general categories of antivirals divided along HIV and
non-HIV medications. Mechanism of viral suppression/antiviral activity by class and
having a good idea of which drugs are in which class, clinical use, toxicity highlights,
mechanism of resistance if it is a ubiquitous drug such as acyclovir- [the HIV
mechanisms of resistance are so numerous, that is should be sufficient to
understand that the virus mutates frequently and resistance is an ongoing and
complex problem.] As for renal dose limitations, you will not likely be asked those
on step 1.
1) Describe why overall antivirals have higher toxicity than antibiotics.
a) This is straight forward. They are intracellular and more invasive than other
drug classes which have extracellular targets.
b) The number of toxicities that involve comorbid conditions is also high
because of the invasive nature of this class of drug.
c) Because of a & b, it is difficult to generalize with regards to toxicities even
within classes of antiviral agents.
2) Compare and contrast antiviral clinical efficacy.
a) Be familiar with agents that possess improved efficacy with less toxicity, but
may have the tradeoffs of costs or limited spectrum of use, or agents that
can be used to combat more than one type of virus (i.e. agents that apply
to HCV but not HBV vs agents which are used for both HIV and HBV)
b) The charts in this review are most useful here

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3) Know common antiviral agent adverse effects and approaches to treatment of
adverse effects.
a) Side effects that need to be managed aggressively vs those which can just
be managed using other treatments for the benefit of antiviral therapy.
Dylipidemias with ARV treatment in HIV are just managed and not usually a
reason to DC drug use, whereas severe lactic acidosis can be
lifethreatening.
b) In other words: do not memorize each and every side effect for each and
every drug, but have awareness of the common ADEs, highlighted
recommendations.
4) Be familiar with major antiviral classes and common specific agents.
a) Dont memorize each and every antiviral agent.
i) For example, you can look up what is in various HIV combination agents,
but its helpful to familiarize yourself with individual classes of agents
because some treatment recommendations recommend treatment by
class combinations.
ii) Most antiviral taxonomy (drug class) centers on where in the viral
replication cycle the drug works.
(1) You might have a drug which is part of HIV, HCV, HBV, and treatment
recommendations because they work at one common point of viral
replication.
(a) For example: direct acting antivirals which are approved for use in
chronic HBV treatment are all nucleot(s)ide analogues.
(i) Lamivudine (Epivir-HBV) approved for HIV and HBV, adefovir
dipivoxil (Hepsera) approved for HBV, entecavir (Baraclude)
approved for HBV, telbivudine (Tyzeka) approved for HBV and
tenofovir disoproxil fumarate (Viread) approved for HIV and
HBV.
1. They all inhibit reverse transcriptase/polymerase activity,
thus decreasing viral replication.
2. They all have black box warnings regarding increased HBV
exacerbation with discontinuation of use, as well as risk of
lactic acidosis and severe hepatomegaly with steatosis.

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5) Explain comorbidity limitations to use of some antivirals.
a) Awareness of toxicities associated with antiviral use should be applied to
assessment of risk with regard to use of specific agents in patients at
increased risk of exacerbation of underlying comorbid diseases.
b) Example: HIV and HBV co-infected patients- you have to consider the effect
on HIV and the effect on hepatic disease as well as resistance in the case of
both. HIV drugs can cause hepatic problems, and both can have variable
effects on resistance of either virus. (This is why the guideline site is very
important for HIV treatment-its ever changing, and no, you dont have to
memorize them, just be aware that this is a challenge in management)
https://aidsinfo.nih.gov
(End Objectives)

D.Antimisiaris 2015
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Practice questions: answers at the end of this document

With regards to HBV treatment in an HIV co-infected patient, which of the following
would you recommend?
a.
b.
c.
d.

Entacavir (ETV)
Tenofovir (TDF)
Emtricitabine/Tenofovir
Lamivudine (LMD)

1. In HIV therapy, Integrase Inhibitors target the enzyme responsible for viral
DNA integration into host DNA. What is the most significant concern when
using this class of drugs?
a. Lactic acidosis
b. Diarrhea, headache, N/V
c. Intracranial hemorrhage
d. Resistance
2. A patient who is being treated for HCV infection becomes pregnant. She has
been receiving PEG Interferon and ribavirin for 8 weeks. She should continue
on this regimen because she responded very well at 4 weeks and only has 4
more weeks to complete this course of treatment.
a. True
b. False
3. Your patient is diagnosed with HCV and now its time to start treatment. You
wish to avoid the use of Interferon because this patient has a history of
suicidal ideation and major depressive disorder. Which of the following
options would you consider?
a. Simeprevir (SIM)
b. Boceprevir (BOC)
c. Sofobuvir (SOF)
d. None of the above
4. There is an H1N1 influenza outbreak and you are getting lots of patients
asking for anti influenza drugs. What medications are options for
treatment?
a. oseltamivir and zanamivir
b. xanamivir
c. Amantadine, Rimantadine, Ostelamivir, and Zanamivir
d. All of the above

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5. Every time your patient goes out in the sun, she gets a herpes outbreak on
her lips. She has been using acyclovir gel to treat the outbreaks but this
time, they are recurring with increased frequency and taking much longer to
heal. Should the strategy for treatment change?
a. We could try penciclovir
b. No, she is just out in the sun more often and changing therapy will
result in treatment failure.
c. We could try oral ganciclovir
d. We could try valciclovir oral

Hepatitis B
Goal of therapy is suppression to undetectable levels to reduce the risk of cirrhosis
and hepatocellular carcinoma. Measures of response: normalization of liver function
tests, HBV seroconversion, decreased evidence of viral replication (HBV DNA IU/mL
decreases).

Usually HBV can resolve spontaneously. (95% of adults recover fully without
complications but younger age of infection results in greater risk of chronic
HBV and greater risk of hepatocellular carcinoma.
Hepatocyte damage occurs due to T cell cytolytic response to lyse infected
hepatocytes
Symptoms of severe liver failure: encephalopathy, coagulopathy (increased
PT/INR), jaundice, ascities, spider angioma, fatigue.

Duration of Therapy: oral antiviral therapy usually is given for 12 months after
seroconversion, but long time follow up is required due to risk of persistence of the
latent virus and many patients ultimately require lifelong therapy.

Special populations:
o HIV coinfection
Vaccinate against HBV (4 intradermal low doses better than 3 IM
standard doses)
Do Not Use Telbivudine (TBD) due to risk of resistance, and avoid
LMD (lamivudine), ETV (entecavir) & AFV (adefovir) due to
increased risk of resistance and therapeutic limitations
Good choices are Tenofovir (TDF) IN COMBINTION with
Emtricitabine (FTC) or other combo products which also contain
FTC in triple combo
o Immunosuppression / Chemotherapy patients
o Liver transplant patients, some regimens more effective than others
o Renal Failure/transplant patients
All oral antiviral agents require dose adjustment in renal
impairment
Vaccination is less effective in this population

D.Antimisiaris 2015
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o

Pregnancy: risk of mother to child transmission which in turn is

associated with high risk of hepatocellular carcinoma in the child.
Antiviral therapy is used
Safety described from use in HIV therapy (LMD, TBD or TDF)
during 3rd trimester
Lactation: safety conditional, consult up to date literature. General
recommendation is breastfeed if mother not on antiviral therapy and
child received proper immunoprophylaxis.
Pediatrics: reserve treatment for severe diagnosis, close monitoring,
LMD and AFV considered safe for use

Strategy to address resistance: resistance may be overcome with switching

agents, combination therapy (adding 2nd agent with a different resistance profile
such as a nucleoside and nucleotide.)
Prevention:

Hep B Immunoglobulin treatment within 48 hours post exposure.

o HBIG=hyperimmune serum globulin.
Vaccination: all infants born in the US after 1991
o Adults at risk born prior to 1991: Healthcare workers, end stage renal
disease patients, Immunocompromised (HIV, Cancer, and Diabetes) or
any adult wishing to be vaccinated.

Interferon: IFN induced host antiviral gene expression to inhibit virus replication,
protein synthesis, and assembly. Also, enhances immune response.

Not for patients with decompensated cirrhosis because results in less

response and increased ADEs.
IFN systems constitute the first line mechanism against viral infection in
humans.
They are induced by viral infection or by double-stranded RNA (dsRNA), a
by-product of viral replication, and lead to the production of a broad range
of antiviral proteins and immunoactive cytokines
Current genetic analyses of many different viruses are revealing an evergrowing number of IFN-antagonistic proteins that target virtually all
components of the IFN system

Oral Medications:
Currently, chronic HBV cannot be cured as can HCV. The reason being that HBV is
a DNA virus which primarily infects hapatocytes nuclear DNA and HBV intrahepatic
DNA is difficult for the current therapy (HBV polymerase inhibitors which are reverse
transcriptase inhibitors RTIs) to get at.
The reason we use reverse transcriptase inhibitors on HBV, a DNA virus, is that HBV
has the peculiarity of replicating via reserve transcription of an RNA intermediate

D.Antimisiaris 2015
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which allows nucleoside reverse transcriptase inhibitors to be effective in controlling
replication of HBV.
-compare and contrast: unlike HCV where medications used for the treatment of
HCV have limited intrinsic and anti-HIV effects, many, if not all HBV medications
demonstrate activity against HIV.
Emergence of resistance to HIV therapy is a concern.

Tenofovir should not be used as monotherapy in HIV co-infected patients due to

potential for resistance of HIV when used alone, but for HBV it is drug of choice with
no HBV resistance noted at 2 years.
A lifelong treatment regimen of tenofovir plus emtricitabine are commonly used,
when lifelong treatment is needed.
Medications Highlights: Antivirals for HBV: see Select Antiviral Tables

Hepatitis C
Goal of therapy is eradication of the HCV.
HCV related glomerular disease is common, and impaired renal function both limits
safety of antiviral drug use as well as presents a comorbid illness to be addressed
during therapy since HCV can worsen renal function.
HCV is an enveloped, positive-sense, single-stranded RNA virus classified within the
genus hepacivirus in the Flaviviridae family.
Currently, HCV isolates are classified into seven major genotypes, i.e., genotypes 1
through 7, and an array of subtypes.
HCV genotypes differ by 20%35% in genome sequence, whereas subtypes within
each genotype can differ by least 15%.
Genotype 1 is the most prevalent (46%), followed by genotype 3 (30%); genotypes
2, 4 and 6 (cumulatively approximately 22%); and genotype 5 (less than 1%).
Different genotypes exhibit distinct geographic distributions:

D.Antimisiaris 2015
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Genotype 1 predominates in America and Europe, genotype 2 in Japan,

genotype 3 in Asia, genotype 4 in Africa and Middle East and genotype 6 in
Southeast Asia.

HCV is transmitted via blood transfusion, intravenous drug abuse, unsafe

therapeutic injection, liver transplantation and other risk factors.
As of now, theres no HCV vaccine: HCV patients should get HBV and HAV
vaccinations if they test + for anti HAV and anti HBVs.
Medication Highlights:
Traditional approach to therapy is using IFN with ribavirin, a synthetic nucleoside
(similar to guanosine).
Ribavirin

Direct inhibition of HCV replication by inhibition of inosine monophosphate

dehydrogenase of the host as well as induction of mutagenesis in the viral
RNA, and immunomodulation by the induction of a T helper 1 type immune
response.
o (dont memorize this level of detail, see summary tables, this is just to
give you an appreciation for the complexity of antiviral action of many
agents)

Interferon (INF): an immune-stimulatory agent. After binding with its receptor on

the surface of cells, INF activates an intracellular signaling cascade which takes the
induction of IFN stimulated genes, establishing non-virus specific antiviral state
inside the cell. Resulting in antiviral proteins promotion.

Interferons (IFN)- PEG or

pegylation of the interferon
allows weekly dosing
(injection) vs daily
Not a

pleasant or preferred
treatment due to flulike
symptoms and depression,
mypopathy, injection site
reactions, malaise and
fatigue, increased liver
function tests, insomnia,
impaired concentration,
irritability, and neutropenia.

IFN is a part of innate immunity against virus

infection.

D.Antimisiaris 2015
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INF can be used alone to treat HCV but typically is used with ribavirin (which is
known for limitations because it causes anemia)
DAAs (Direct Acting Antivirals as opposed to interferon)
Recently, the use of active direct-acting antiviral molecules to block HCV infection
has led to substantial improvements in sustained virological response rates in
genotype 1-infected patients.
However, IN THE FUTURE, JUT FYI, the use of these drugs may allow selection of
resistant variants if direct-acting antiviral monotherapy is adopted, and a high
relapse rate occurs after direct-acting antiviral treatment is discontinued.
Special Considerations in Treatment:

Ribavirin is an RNA polymerase inhibitor, which inhibits synthesis of guanine

nucleotides by competitively inhibiting inosine monophosphate
dehydrogenase.
Ribavirin is a common part of HCV therapy but has a serious limitation with
risk for hemolytic anemia
Ribavirin is specifically contraindicated in pregnancy (men and women) due
to teratogenic/embryocidal effects. Multiple dose half-life is 12 days and may
persist for 6 months.
Avoid breast feeding with ribavirin containing regimens
INF+Ribavirin is the cornerstone of most HCV therapy. Protease inhibitors
(boceprevir and simeprevir), are added to INF and Ribavirin for some
genotypes (dont memorize which genotypes are specifically treated with
which regimen because it changes frequently, just know where to look it up
for when you need to-like on clinical rotations)
o Protease inhibitors easily develop resistance, thus they should never
be used as monotherapy.

Medications Highlights:
A detailed table of HCV treatments accompanied soft chalk on antivirals for your
reference.
Key Points:

Combination Direct Acting antivirals (non- ribavirin type) are able to achieve
sustained virologic response (SVR) 12 weeks after discontinuation of therapy,
of >95%. *which studies have shown is an indicator that 6 month SVR will
occur.
o In other words, these are successful interferon free regimens.
o RVR (rapid viral response to therapy) is best predictor of SVR.

D.Antimisiaris 2015
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Ideal is to avoid IFN and ribavirin (i.e using oral combination therapy see
chart).
Refer to guidelines at time of treatment decision- genotype, relapse, and
futility rules impact decisions. They are complex as in HIV.
o Futility rules means for example if you have a patient on triple therapy
( PEG INF + ribavirin + beoceprevir) and you test HCV RNA and the
level at treatment week 12 of >100IU/mL or detectable at TW24 then
you would DC triple therapy.
o Complex recommendations: example

Be familiar with various drugs ADEs and thats enough for now, dont
memorize guidelines.

PEG Interferon + ribavirin

Ribavirin (RBV)
RNA polymerase inhibitor

Contraindication: pregnancy due to

ribavirin combo
ADEs: flu like symptoms, fatigue, HA,
Chills, myalgia, rash, depression,
irritability, anxiety, insomnia
Never used as monotherapy
Contraindication: pregnancy,
hemoglobinopathy (thalassemia, sickle
cell)
ADEs: hemolytic anemia, fatigue, HA,
insomnia, pruritus
Drug Interactions: multiple HIV med
interactions, increased risk of lactic
acidosis.
May consider erythropoietin stimulating
agent for mild anemia

Directacting Antiviral Agents: HCV Protease (NS3/4A eg. paritaprevir) & NS5B polymerase nucleotide.
Combined with PEGIFN & RBV in HCV genotype 1 to SVR rates from ~40% to ~7095% & decrease length of
therapy, but AE as compared to
interferon sparing regimens. Interferon sparing regimens may be considered if: PEGI intolerance, other
concomitant auto immune disorders, decompensated liver dx, severe depression, decrease neutrophils/Hgb or
cardiovascular dx. (FYI dont memorize)

Boceprevir (BOC)

Contraindication: Monotherapy,
concurrent therapy with high risk
medications (i.e. antiarrhythmics, and
others which result in severe ADEsstatins and myopathy)

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Simeprevir (SIM)

Telaprevir (TVR)

Multiple drug interactions (cyp 3A4

especially)
ADEs: anemia, neutropenia, dysguesia,
fatigue, nausea and chills.
Contraindication: Monotherapy
ADEs: rash (sulfa), photosensitivity,
elevated bilirubin.
Drug Interactions: cyp 3A4 substrate
caution with narrow therapeutic window
meds.
May soon be DCd by company due to
ADEs (anemia and Stevens Johnson
Syndrome), strong 3A4 inhibitor.

NS5B nucleotide (eg. Sofosbuvir) & nonnucleoside (eg. Dasabuvir) polymerase inhibitors
and combo products

Sofobuvir (SOF)
Sovaldi

Ledipasvir (LDV) + SOF

Harvoni

More combinations entering market at

this time
Main concepts:

Contraindication: Monotherapy
ADEs: fatigue, HA, Nausea, Insomnia,
Neutropenia
Drug Interactions: p-gp substrate:
anticonvulsants and rifampin, tipranavir
and ritonavir can decrease SOF levels.
Caution with Amiodarone (decreased
HR) $50K for 12 weeks
Fatigue, HA, N/V/D, insomnia, may
increase glucose, bilirubin
Same drug interactions as Sovaldi
plus proton pump inhibitors
(omeprazole etc) and H2 blockers
(ranitidine) can change gastric pH and
alter absorption of LDV.
NOTE- not a monotherapy
$94K 12 weeks, $189K for 24 weeks
Just be aware for later

Monotherapy is not acceptable for direct acting antiviral agents in

treatment of HCV due to resistance.
INF has troublesome side effects
Ribavirin has serious contraindications and side effects

HIV Treatment
95% adherence to regimen is required to slow resistance

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Individualize thereapy with respect to comorbidities (CV, Liver, Renal dxs;

psych hx, TB, chemical dependence), pt. compliance, convenience, ADEs and
drug interactions.
Requires management by HIV expert
Initial therapy: 3 drug regimen (not to be memorized, see guidelines they
change frequently and address specific situations) examples include 2 NRTIs
+ 1 NNRTI or boosted PIs or integrase inhibitor.
Management of common ADEs
Diarrhea (ARV induced)

Rule out infections or medical causes before chronic treatment of ADE

Loperamide, diphenoxylate and codeine useful (dont memorize for this
exam) just know that this ADE is benign enough to try to manage
rather than DC HIV treatment.
o Everything in medication management comes down to riskbenefit analysis
Other options: oat bran, psyllium, pancrelipase caps

Nausea: multiple causes, taste, GI motility decreases, chemotrigger zone

stimulation, often resolves a few weeks into advent of therapy. Can treat
with ginger, or other NV treatments.
Rash: common for rash to occur with advent of new treatment and if not
resolving after one week, monitor. Some rash are signs of a serious ADE.

Abacavir, if refractory and includes fever, BI upset, malaise, muscle or

bone pain and cough, SOA and sore throat, stop abacavir and do not
restart.
Nevirapine: start with low dose to minimize risk of serious reaction.
For common, not serious rash, treat with antihistamines and if
necessary corticosteroids.

See chart HIV treatment table for medication highlights

Refer to https://aidsinfo.nih.gov/contentfiles/lvguidelines/PerinatalGL.pdf for
info regarding use in pregnancy. ARVs started after 14 weeks(& by 28weeks)
significantly decreases mother to child transmission (mtct); intrapartum ARV
+ infant ARV prophylaxis (6wk) essential to decrease mtct transmission.

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Influenza
Vaccination is the main antiviral defense. Especially: healthcare workers,
high risk patients such as the elderly.

Efficacy, prevents 70%

Protection begins 2 weeks post vaccination and persists about 8
months
Fumist (non -injection vaccination) preferred in healthy 2-6 year olds
Monitor 15-30 minutes post vaccine for reaction
Contraindicated in severe egg allergy patients or persons who had
previous severe reactions, those who have had sever acute febrile
illness before, GBS (Guillian Barre syndrome) reaction within 6 weeks
post vaccination

Antiviral agents for influenza treatment can help within 48 hours of

symptoms to shorten course by approximately a day and relieve symptoms
to some extent.

Treat persons with severe illness or those likely to suffer complications

or death due to influenza.
o Also encourage fluids, rest and analgesics
For persons not at high risk, they dont require antiviral meds for
treatment or prophylaxis.

Antiviral Influenza Agents

M2 Inhibitors:
Inhibit un-coating
of the virus after
invasion of host
cell

Route of
administrat
ion
Dosage
Forms
Prophylaxis
Treatment

Neuraminidase Inhibitors (NIs)

Interferes in the budding off of new viral
particles ready to spread after initial host
infection (have to use early in infection
to work)

Amantadine
Rimantadine
(analog of
amantadine)
Oral

Oseltamivir (Tamiflu)

Zanamivir
(Relenza)

Oral

Oral Inhalation
(<2% oral
bioavailability)

Capsules, syrup

Capsules, powder for

suspension
Yes >1yr old

disk haler

Yes >1yr old

Yes >7 yr old

No: lots of
resistance
No: resistance

Yes >7 yr old

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Renal dose
adjustment
ADEs

Comments

>99% except if
severe H5N1 may
combo thx w NI
Yes
Multiple because
of pro-dopamine
effects, CNS,
irritability,
insomnia,
dizziness, GI
upset
Better CNS
toxicity with
reimantidine
Helps in
institutional
outbreaks
(nursing homes)
to prevent spread
of influenza.
Avian isolates are
resistant to
amantadine
Overall not used
much due to
resistance

Yes

No

Nausea/V/insomnia,
bronchitis, HA,
elevated LFTs
Behavior changes in
kids
Probenecid increases
levels

May cause
bronchospasm in
asthma or COPD
patients (dry
powder
formulation)

People stockpile for

avian and swine flu
(H5N1 and H1N1)

People stockpile
for avian and
swine flu (H5N1
and H1N1)
*Pramivir, an IV
agent is more
potent than
zanamivir against
H1N1 Influenza A.

NOTE: This information can change from year to year, especially with regards to H1N1
and other rapidly changing viruses.

Other Antiviral Agents

Herpes-simplex viruses
HSV-1 (oral herpes)
HSV-2 (genital herpes)
Human herpesvirus/VZV
Chickenpox and shingles (HHV-3 or VZV)

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Epstein-Barr (HHV-4) aka EBV infection

Cytomegalovirus (HHV-5) aka CMV infection
Kaposis sarcoma (HHV-8)
Respiratory Syncytial Virus: in adults and older healthy children=mild cold
like symptoms

In babies can cause pneumonia, severe breathing problems and

premature babies or those with other health problems are at high risk.

Miscellaneous Antiviral Agents

Synthetic nucleoside analogs to treat HSV1,2, VZV or HHV3
Acyclovir (Zovirax)
Guanosine analog
convereted by viral
thymidine kinase in infected
cells to acyclovir
monophosphate and then to
triphosphate. Acyclovir
triphosphate competes with
endogenous substrates for
biding to viral DNA
polymerase and when
incorporated to growing
DNA chair, further synthesis
halts. Very specific for viral
DNA
PREFERENTIALLY INHIBITS
VIRAL DNA POLYMERASE

Valacyclovir
Prodrug formulation of
acyclovir, rapidly and
completely converted
to active form.
SAME MOA as acyclovir
Penciclovir
(Denavir)
SAME MOA as acyclovir

Famciclovir

Oral, topical and

parenteral forms

Resistance is common
Well tolerated rare CNS
side effects

Same, same as
acyclovir. Simplified
dosing and more costly
Oral valacyclovir
bioavailability if just
about like IV: prodrug of
acyclovir
Poor oral availability:
only topical formulation
-used if topical and oral
together fail
(valcyclovir and
acyclovir)
Prodrug of penciclovir

Same, same.

Not as much
resistance.

Used for recurrent HSV,

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(Famvir)
SAME MOA as acyclovir

with good oral

absorption
Prodrugs are typically
aimed at improved
absorption and PK, PD.
Treatment of CMV, and other misc. agents
Ganciclovir
Oral doses for
(Cytovene)
suppression
Guanine analog which
IV doses for treatment
results in DNA chain
Intravitreal
termination within
device can be
infected cells.
implanted into
the eye to treat
CMV in eye.
10 times more
potent when
compared to
acyclovir for CMV
Valganciclovir
(Valcyte)
Prodrug of ganciclovir
Foscarnet
(Foscarvir)
Inorganic
pyrophosphate which
binds and inactivates
DNA polymerase
without requirement of
phosphorylation by
thymidine kinase (as in
acyclovir type)
Cidofovir (Vistide)
Acyclic nucleoside
derivative
Also doesnt require
phosphorylation by
thymidine kinase for
activation

May allow for PO

treatment of CMV
Wide spectrum activity:
HSC1, HSV2, CMV,
Influenza A, Influenza
B, HIV, HBV.

and VZV

Neutropenia occurs 3040% in immune

suppressed patients.
Cannot use in pregnant
or those at risk of
pregnancy
Useful esp. in CMV
infections in HIV and
solid organ transplant
patients who are at
higher risk of CMV
infection.
Same, same

Significant dose limiting

renal toxicity

Utilized after resistance

to CMV and HSV
treatement

Has role in resistant

cases
HSV1, HSV2, VZV, EBV,
CMV
Only IV available

Nephrotoxic
Recommended prehydration with normal
saline (IV NS) and
adding oral probenecid
just prior to
administration of
cirofovir (probenecid
blocks kidney

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concentration of other
drugs)
Drugs used to treat Respiratory Syncytial Virus Infections (RSV)
Ribavirin
RSV, Influenza A, and B Multiple toxicities (see
Hep c drugs): nausea,
anemia, lethargy
Palivizamab
RSV
Hypersensitivity
(Synagis)
Only used in children
Thrombocytopenia
Binds to A antigenic
Rash
site of RSV F protein
Fever
Is a Monoclonoal
Antibody

Answers to practice questions

6. With regards to HBV treatment in an HIV co-infected patient, which of the
following would you recommend?
e. Entacavir (ETV)
f. Tenofovir (TDF)
g. Emtricitabine/Tenofovir
h. Lamivudine (LMD)
Answer: ETV has no efficacy against HIV, plus it can increase ARV therapy
resistance; Lamivudine has very high resistance levels and is not first line (might be
used if all other options fail due to toxicity or resistance), Tenofovir should not be
used as monotherapy due to increased risk of HIV resistance, therefore C
tenofovir combined with the NRTI emtricitabine is the best choice.

7. In HIV therapy, Integrase Inhibitors target the enzyme responsible for viral
DNA integration into host DNA. What is the most significant concern when
using this class of drugs?
a. Lactic acidosis
b. Diarrhea, headache, N/V
c. Intracranial hemorrhage
d. Resistance
Answer: b, Diarrhea, HA, N/V

8. A patient who is being treated for HCV infection becomes pregnant. She has
been receiving PEG Interferon and ribavirin for 8 weeks. She should continue
on this regimen because she responded very well at 4 weeks and only has 4
more weeks to complete this course of treatment.
a. True
b. False

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Answer: False, ribavirin is contraindicated in pregnancy

9. Your patient is diagnosed with HCV and now its time to start treatment. You
wish to avoid the use of Interferon because this patient has a history of
suicidal ideation and major depressive disorder. Which of the following
options would you consider?
a. Simeprevir (SIM)
b. Boceprevir (BOC)
c. Sofobuvir (SOF)
d. None of the above
Answer: d, none of the above because monotherapy with direct acting agents if not
recommended.

10.There is an H1N1 influenza outbreak and you are getting lots of patients
asking for anti influenza drugs. What medications are options for
treatment?
a. oseltamivir and zanamivir
b. xanamivir
c. Amantadine, Rimantadine, Ostelamivir, and Zanamivir
d. All of the above
Answer: all of the above can work for H1N1
11.Every time your patient goes out in the sun, she gets a herpes outbreak on
her lips. She has been using acyclovir gel to treat the outbreaks but this
time, they are recurring with increased frequency and taking much longer to
heal. Should the strategy for treatment change?
a. We could try penciclovir
b. No, she is just out in the sun more often and changing therapy will
result in treatment failure.
c. We could try oral ganciclovir
d. We could try valciclovir oral
Answer: d-try oral valacyclovir because she is using topical acyclovir as of
now, and she can next add oral therapy which is a bit more potent using
acyclovir or valacyclovir. She shouldnt use ganciclovir due to toxicity and
that its indicated for CMV, b is just not accurate, a penciclovir would be a
next step if she seems to have resistant virus to oral and topical acyclovir
products.