Antiviral preparations

Virus is a microscopic particle, consisting of proteins and nucleic acids, that is able to infect cells of living organisms. Viruses are obligate parasites meaning that they can not multiply outside the living cells. They do not have their own metabolic system and their growth and replication depends on the host cells. There are known viruses that multiply in the cells of plants, animals, fungi and bacteria (bacteriophages). Viruses are the molecules of nucleic acids (DNA or RNA) enclosed in a protective protein shell (capsid).Viruses contain only one type of nucleic acid: either DNA or RNA.

The mechanism of infection of viral life cycle includes the following mechanisms:

  1. Viral particle binds to the host cells by linking its capsules glycoproteins to specific receptors on the surface of cells
  2. Penetration of viral particle into the host cells.
  3. Uncoating (opening) of viral capsule close to nuclear pores and movement of viral DNA (genetic materia) into the nucleus.
  4. Synthesis of nucleic acid for production of DNA (replication of genetic material) and RNA (protein synthesis). These proteins act as viral enzymes that catalyze viral replication, as capsomers or participate in formation of coat or incorporate into host cells.
  5. Assembling of individual components into the new viral particle
  6. Release of new cells and contamination of new host cells

The treatment of viral infection is targeted to different viral life-cycles. Currently there are several groups of anti-viral drugs with deferent action mechanisms.

Nucleosides - Acyclovir, Valacyclovir, Famciclovir, Gamciclovir. Chemical structure of this group of medicines is close to purine nucleoside deoxyguanosine - DNA component. Under the action of thymidine kinase produced by viruses, necleosides inter the affected host cells and blocks the enzyme DNA polymerase necessary for viral DNA replication. The preparations selectively act on synthesis of viral DNA and do not significantly affect DNA replication of host cells. Nucleosides are used to treat: Herpes Simlex type 1 and type 2, Varicella-Zoster, Herpes Labialis, Epstein-Barr virus, cytomegalovirus.

Cyclic amines (adamantanes) include such preparations as Amantadine and Remantadine. Amantadine affects the replication of influenza A viruses. The release of influenza A viruses require protons from the acidic content. Cyclic amines work by channel protein in the viral wall that permits influx of proton. By blocking protein channels cyclic amines prevent the "uncoating" of viral capsule. Cyclic amines also suppress viral maturation.

Neuraminidase inhibitors include Zanamivir, Oseltamivir, Peramivir. Neuroaminidase is a key enzyme involved in replication of replication of influenza A and B viruses. The inhibition of neuraminidase interfere with penetration of viruses into the host cells, release of virions from infected cells, decreasing the resistance to the inactivating action of mucous secretion of the respiratory tract. All of this leads to decrease of viral spread in the organism. In addition, neurominidase inhibitors reduce production of certain cytokines, preventing the development of local inflammation and impairing the systemic reactions of viral infection (fever, etc.). This group of medicines does not act on other types of viruses.

Drugs used for AIDS (HIV) treatment
HIV virus is not susceptible to targeted intervention, because different metabolic processes occur in infected cells. At first viral RNA must be converted into DNA. This stem is catalyzed by viral "reverse transcriptase." Doublestranded DNA is incorporated into the host genome with the help of viral integrase.

The group of medicines used for HIV treatment can be divided into the following:
I)Inhibitors of reverse transcriptase.
a)Nucleoside agents

  • Thymine analogues (azidothymidine, stavudine)
  • Cytoside analogues (lamivudine, zalcitabine)
  • Guanine (Carbovir, Abacavir)

This group of medicines works by inhibiting reverse transcriptase which is necessary for transcription of viral RNA into DNA.
b) Non-nucleside agents (nevirapine, delavirdine, efavirenz). They selectively bind to reverse transcriptase and prevent it from adopting the active conformation. This inhibition is non competitive.

II) Protease inhibitors - Saquinavir, Idinavir, Ritonavir, Darunavir, Amprenavir, Atazanavir, Fosamprenavir, Lopinavir, Nelfinavir, Tipranavir. Viral protease is enzyme that breaks down proteins precursor into proteins required for viral replication. By inhibiting protease this group of medicines suppress HIV replication.

For the purpose of increasing the effectiveness of HIV treatment and preventing the development HIV viruses resistance, the treatment approach is focused on combined therapy of reverse transcriptase inhibitor with each other or with protease inhibitors.

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