Page 878 - Basic _ Clinical Pharmacology ( PDFDrive )

864 SECTION VIII Chemotherapeutic Drugs

ACRONYMS & OTHER NAMES ■ AGENTS TO TREAT HERPES
3TC Lamivudine SIMPLEX VIRUS (HSV) &
AZT Zidovudine (previously azidothymidine) VARICELLA-ZOSTER VIRUS (VZV)
CMV Cytomegalovirus
CYP Cytochrome P450 INFECTIONS
d4T Stavudine Three oral nucleoside analogs are licensed for the treatment
ddC Zalcitabine of HSV and VZV infections: acyclovir, valacyclovir, and fam-
ddI Didanosine ciclovir. They have similar mechanisms of action and compa-
EBV Epstein-Barr virus rable indications for clinical use (see Table 49–1); all are well
FTC Emtricitabine tolerated.
Comparative trials have demonstrated similar efficacies of
HBeAg Hepatitis e antigen these three agents for the treatment of HSV, with shortening
HBV, HCV Hepatitis B virus, C virus of the duration of symptoms by approximately 2 days, the time
HHV-6, -8 Human herpesvirus-6, human herpesvirus-8 to lesion healing by 4 days, and the duration of viral shedding
HIV Human immunodeficiency virus by 7 days in first episodes of genital herpes and shortening of
HSV Herpes simplex virus the overall time course by 1–2 days in recurrent genital herpes.
INSTI Integrase strand transfer inhibitor Treatment of first-episode genital herpes does not alter the
NNRTI Nonnucleoside reverse transcriptase inhibitor frequency or severity of recurrent outbreaks. Long-term sup-
pression with antiherpes agents in patients with frequent recur-
NRTI Nucleoside/nucleotide reverse transcriptase inhibitor rences of genital herpes decreases the frequency of symptomatic
PI Protease inhibitor recurrences and of asymptomatic viral shedding, thus decreasing
RSV Respiratory syncytial virus the rate of sexual transmission. However, outbreaks may resume
SVR Sustained viral response upon discontinuation of suppression. The efficacy of the anti-
UGT1A1 UDP-glucuronosyltransferase 1A1 herpes agents in orolabial herpes is generally less than that in
VZV Varicella-zoster virus anogenital herpes.

Blocked by
enfuvirtide (HIV); Blocked by
docosanol (HSV), amantadine,
maraviroc (HIV), rimantadine
palivizumab (RSV) (influenza)

Viral Penetration
attachment
and entry Uncoating
Blocked by
interferon-alfa
(HBV, HCV)
Blocked by NRTIs,
Mammalian Nucleic acid NNRTIs (HIV),
cell synthesis Nucleoside/nucleotide
Blocked by analogs (HSV, HBV)
neuraminidase
inhibitors Packaging
(influenza) and Integration
assembly (retroviruses)
Viral Transcription
release
Viral protein
synthesis Blocked by INSTIs (HIV)

Blocked by PIs
(HIV, HCV)

FIGURE 49–1 The major sites of antiviral drug action. Note: Interferon alfas are speculated to have multiple sites of action. (Modified and
reproduced, with permission, from Trevor AJ, Katzung BG, Masters SB: Pharmacology: Examination & Board Review, 9th ed. McGraw-Hill, 2010. Copyright © The McGraw-Hill
Companies, Inc.)