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It should be appreciated that even experienced clinicians are still on a learning curve with the prevention and treatment of most viral infections using antivirals. Also a prodrug of aciclovir called valaciclovir has been developed. This is the L-valine ester of aciclovir and after absorption undergoes almost complete hydrolysis to aciclovir and the essential amino acid L-valine.

Valaciclovir itself has negligible pharmacological activity and all products of its metabolism except for aciclovir are inert or well characterized. Of course the most important product of its metabolism is aciclovir itself. Similar in concept is the clinical application of the prodrug famciclovir which is converted enzymatically in the patient to the active anti-herpes nucleoside analogue drug penciclovir Figure 4. Aciclovir is used as a prophylactic, before surgery for example, to prevent recurrent herpes type I infections in bone marrow and heart transplant patients, and therapeutically to prevent spread of mucocutaneous infections in already infected and immune compromised persons.

It has also been shown to be very effective in saving lives when used to treat herpes encephalitis. Aciclovir is also used against recurrent HSV infections, particularly those of the genital tract, and to a lesser extent in various forms of VZV infections. More effective against VZV is the prodrug of aciclovir, valaciclovir which is better absorbed orally and is rapidly converted to aciclovir in vivo.

However, unlike aciclovir the drug induces rather severe neutropenia and thrombocytopenia. Foscarnet, which is not a nucleoside analogue, can be used to treat intractable cases of CMV but the drug is administered in hospitals under close clinical care. It has little or no effect against cellular DNA polymerase. However, a latently infected cell cannot be cured and thus aciclovir does not eradicate herpesvirus from an infected individual, but it can be used to prevent clinical recurrences.

The compound has proved to be remarkably safe in clinical practice and some patients have taken the drug orally daily for several years. Another nucleoside analogue closely related to aciclovir and called penciclovir is widely used in clinical practice, with an advantage that fewer daily doses are required. As with the prodrug valaciclovir, a prodrug of the new molecule has been introduced called famciclovir Figure 4.

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This prodrug may also have clinical usefulness against hepatitis B virus. It had in fact been synthesized as a potential explosive and not as a biological. A very similar molecule but with an extra methyl group attached rimantadine has equivalent clinical activity but causes rather fewer side-effects. Studies of the therapeutic use of amantadine in prisons, schools and universities throughout the world showed, perhaps surprisingly, that if the drug was given after infection but within 24—48 hours of the onset of symptoms these resolved more quickly and the number of days of incapacity was reduced.

Thus therapeutic use of a drug against a respiratory virus is possible, and this opportunity, unexpected at the time, has been exploited by the newer antineuraminidase drugs. Prophylactic use should continue daily for up to 4—5 weeks until the epidemic has passed. Clinicians now appreciate that amantadine dosage must be carefully adjusted for elderly and frail individuals and particularly those with kidney disease or urinary retention, in whom the drug could accumulate.

A reduced dose of mg or lower daily is recommended. The mode of action of the drug is still the subject of research and the principal viral target is the viral M2 protein. The M2 protein forms a transmembrane ion channel in the virus and amantadine can block this channel much as a gate can prevent access to the entrance of a building. All these vital early stages of viral uncoating are blocked by amantadine when it sits in the ion channel and blocks off access for protons.

It is no surprise that drug resistance to amantadine occurs when mutations in the M2 gene and subsequent amino acid substitutions in the M2 protein prevent the binding of the molecule and hence stop its effect as a gate. Both drugs bind to a group of 11 or so amino acids in the active site of the NA enzyme. Even previous pandemic viruses such as the Great Pandemic of have a near identical active site and are inhibited.

Drug-resistant mutants have been described but to date appear less pathogenic and less infectious than the wild-type virus and thereby would not be expected to spread in the community. The drug is rapidly absorbed after oral administration with a short 1 hour half-life and so the drug is given two or three times daily.

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Zidovudine is now considered to be useful for prolonging the life of these patients for up to 1 year, but its use is enhanced by drug combinations. However, headaches, nausea and insomnia are not uncommon side-effects of the drug and the patients have to be carefully monitored. The dideoxynucleoside monophosphate is phosphorylated to the triphosphate, by cellular enzymes, and the triphosphate differentially inhibits the viral reverse transcriptase enzyme and has lesser effects on the cellular DNA polymerase.

Unfortunately the phosphorylation to the active triphos- phate occurs not only in virus-infected cells but also in normal cells, and this explains the side-effects of the drug. In contrast, as we have noted above, aciclovir triphosphate is only present in herpes-infected cells.

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Also effective are non-nucleoside analogue inhibitors of viral reverse transcriptase and particularly inhibitors of other viral target enzymes such as protease. Undoubtedly a clinical breakthrough has been the development of the two prodrugs, valaciclovir and famciclovir, to treat herpes infections. Fortunately drug resistance is not likely to be a major problem with herpesviruses. There also remain some very important target viruses against which few, if any, antivirals exist. Threats of bioterroism will lead to evaluation of drugs against smallpox such as cidofovir and against viruses which cause haemorrhagic fevers such as Lassa and Ebola.

Principles and Practice of Clinical Virology

Four decades ago the discovery of what we now recognize as important cytokines, a and b interferon, led to over-hasty conclusions that viruses could be conquered by these broad spectrum molecules. Additional achieve- ments during the 20th century have been the introduction of many new virus vaccines, e. Vaccines against e. Great optimism followed the successful smallpox programme, but not all infectious diseases of viral aetiology may be so amenable to control. Nevertheless, there is a range of virus diseases within reach of being controlled by vaccination at least in developed countries.

Poliomyelitis is for all practical purposes eliminated from many countries through extensive use of either live attenuated or killed inactivated vaccines among children. In some developed countries measles is now close to eradication or is an extremely rare disease, and through continued mass vaccination mumps and rubella may also become infections of the past. It is notable that those virus infections which have been well controlled by immunization are systemic infections in which a viraemia is an essential component of the pathogenesis of the disease. This latter problem may well apply to the development of HIV vaccines.

With some vaccines e.

Adjuvants, usually aluminium salts, can also delay the release of vaccine material from the injection site. In the case of non-replicating vaccines the virus may be replicated in an appropriate laboratory system, e. Hepatitis B vaccine is non-replicating and obtained by the expression in yeast of cloned viral genes.

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To date, emphasis has been placed on live virus vaccines except where laboratory replication has not been possible hepatitis B or satisfactory attenuation has not been achieved rabies. Less antigenic mass is required in a live virus vaccine since there is replication and build-up of immunogen in the vaccinee. As a consequence inactivated vaccines are usually more expensive. Live virus vaccines induce long-lasting immunity after a single dose live poliovirus vaccine requires three doses to ensure protection against all three types ; killed vaccines often require multiple doses. Live virus vaccines also have their drawbacks.

Through the manufacturing process adventitious agents may be incorporated. Attenuated vaccine strains may revert to virulence on passage through the human host. Finally, attenuation is judged in immunocompetent individuals, therefore live vaccines are often contraindicated in immuno- compromised individuals and also during pregnancy. The initial hope for a HIV vaccine was precisely that: to confer complete protection sterilizing immunity and thus arrest the virus at the site of entry. This may indeed be a formidable task. However, there is abundant evidence that many vaccines elicit an excellent protection against disease.

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A good example of such a case is the use of inactivated poliovaccines that in some Scandinavian countries has managed to eliminate poliomyelitis, even if the post-vaccination intestinal immunity has been low or absent. Passive immunization is the transfer to one individual of antibodies formed in another. The advantage is that it is rapid in onset effective within a day , but it has the disadvantage of being short-lived lasting only 2—6 months since the injected foreign antibody decays with a half-life of 21 days. Human immunoglobulin preparations are made of donated blood through a series of fractionation steps.

Hyperimmune globulins are made from a pool of units of blood selected because they have a high titre of a particular antibody. Such preparations are available for the prevention of hepatitis B, rabies and chickenpox. In certain situations rabies, neonatally acquired hepatitis B it is possible to combine active and passive immunization and take advantage of the best features of each, the immunoglobulin giving immediate protection until lasting active immunity from vaccination develops.

Live polio vaccine is always given by mouth. Injectable vaccines are usually administered intra- muscularly or deep subcutaneously, although an equally effective but smaller dose can sometimes be given intradermally and this may be relevant with expensive vaccines e. Since vaccination usually requires attendance at a clinic it is often worthwhile giving more than one vaccine at a visit. Individuals can respond to multiple antigens administered simultaneously, although between 4 and 14 days after one vaccine individuals may respond poorly to another.

Therefore vaccines should either be given simultaneously, preferably at different sites, or after an interval of at least 3 weeks.