Undecylenic acid is 10-undecenoic acid. The drug is fungistatic against a variety of fungi, including those that cause ringworm. Undecylenic acid (desenex, others) is available in a foam, ointment, cream, powder, spray powder, soap, and liquid. Zinc undecylenate is marketed in combination with other ingredients. The zinc provides an astringent action that aids in the suppression of inflammation. Compound undecylenic acid ointment contains both undecylenic acid (~5%) and zinc undecylenate (~20%). Calcium undecylenate (caldesene, cruex) is available as a powder.
Undecylenic acid preparations are used in the treatment of various dermatomycoses, especially tinea pedis. Concentrations of the acid as high as 10%, as well as those of the acid and salt in the compound ointment, may be applied to the skin. The preparations usually are not irritating to tissue, and sensitization is uncommon. in tinea pedis, the infection frequently persists despite intensive treatment and the clinical "cure" rate is at best ~50%. Other agents therefore are preferred. Undecylenic acid preparations also are approved for use in the treatment of diaper rash, tinea cruris, and other minor dermatological conditions.
For a complete Bibliographical listing see Goodman & Gilman's The Pharmacological Basis of Therapeutics, 11th ed., or Goodman & Gilman Online at www.accessmedicine.com.
Viruses are obligate intracellular parasites that contain either double- or single-stranded DNA or RNA enclosed in a protein coat called a capsid. Some viruses also possess a lipid envelope that, like the capsid, may contain antigenic glycoproteins. Most viruses contain or encode enzymes essential for viral replication inside a host cell, and they usurp the metabolic machinery of their host cell. Table 49-1 outlines the stages of viral replication and the classes of antiviral agents that act at each stage of replication. Effective antiviral agents inhibit virus-specific replicative events or preferentially inhibit virus-directed rather than host cell-directed nucleic acid or protein synthesis.
Figure 49-1 provides a schematic diagram of the replicative cycle of a DNA virus (A) and an RNA virus (B). DNA viruses include poxviruses (smallpox), herpesviruses (chickenpox, shingles, oral and genital herpes), adenoviruses (conjunctivitis, sore throat), hepadnaviruses (hepatitis B virus [HBV]), and papillomaviruses (warts). Typically, DNA viruses enter the host cell nucleus, where the viral DNA is transcribed into messenger RNA (mRNA) by host cell polymerase and mRNA is translated into virus-specific proteins.
For RNA viruses, replication in the host cell relies either on enzymes in the virion (the whole infective viral particle) to synthesize its mRNA or on the viral RNA serving as its own mRNA. The mRNA is translated into various viral proteins, including RNA polymerase, which directs the synthesis of more viral mRNA and genomic RNA (Figure 49-1B). Most RNA viruses complete their replication in the cytoplasm, but some, such as influenza, are transcribed in the host cell nucleus. RNA viruses include rubella virus (German measles), rhabdoviruses (rabies), picornaviruses (poliomyelitis, meningitis, colds, hepatitis A), arenaviruses (meningitis, Lassa fever), flaviviruses (West Nile meningoencephalitis, yellow fever, hepatitis C), orthomyxoviruses (influenza), paramyxoviruses (measles, mumps), and coronaviruses (colds, severe acute respiratory syndrome [SARS]).
Retroviruses are RNA viruses that cause diseases such as acquired immunodeficiency syndrome (AIDS) (see Chapter 50) and T-cell leukemias (human T-cell lymphotropic virus I [HTLV-I]). They contain a reverse transcriptase that makes a DNA copy of the viral RNA template. The DNA copy integrates into the host genome, at which point it is referred to as a provirus and is transcribed into both genomic RNA and mRNA for translation into viral proteins. The polymerase of hepad-naviruses possesses reverse transcriptase activity.
Although many compounds show antiviral activity in vitro, most affect some host cell function and are associated with unacceptable toxicity. Effective agents typically have a restricted spectrum of antiviral activity and target a specific viral protein, most often an enzyme involved in viral nucleic acid synthesis (polymerase or transcriptase) or a viral processing protein (protease). Single-nucleotide changes leading to critical amino acid substitutions in a target protein often can cause resistance to antiviral drugs. Most agents inhibit active replication, so viral replication may resume following drug removal, and effective host immune responses are essential for recovery from infection. Clinical failures of antiviral therapy may occur with drug-sensitive virus in immunocompro-mised patients or following emergence of resistant variants. Most drug-resistant viruses are recovered from immunocompromised patients or those with chronic infections (e.g., HBV) with high viral loads and repeated or prolonged courses of antiviral treatment. Antiviral agents do not eliminate nonreplicating or latent virus, although some drugs are used effectively for chronic suppression of disease reactivation. Clinical efficacy requires inhibitory concentrations at the site of infection, usually within infected cells. For example, nucleoside analogs must be taken up and phosphorylated intracellularly for activity; consequently, concentrations of critical enzymes or competing substrates influence antiviral effects in cells of different types and in different metabolic states. In vitro sensitivity tests for antiviral agents generally are not standardized, and results depend on the assay system, cell type, viral inoculum, and laboratory. Therefore, clear relationships among drug concentrations active in vitro, those achieved in blood or other body fluids, and clinical response are not established for most agents.
Table 49-2 summarizes currently approved antiviral drugs.
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