Здесь вырезка из статьи -одного из лучших специалистов мира по поиску антивирусных компонентов. Я его встретил в Праге впрошлом году во время курса его лекций. Переводить времени нет, извиняйте.
α-herpesvirus infections
The α-herpesviruses include herpes simplex virus
types 1 and 2 (HSV-1 and HSV-2) and varicella–zoster
virus (VZV). They can cause both primary infections
(for example, HSV-1 causes gingivostomatitis,
encephalitis and eczema herpeticum, HSV-2 causes
genital and neonatal herpes, and VZV causes varicella
(chicken-pox)) and recurrent infections (for example,
HSV-1 causes herpes labialis and herpetic keratitis,
HSV-2 causes genital herpes and VZV causes herpes
zoster). These viruses can also cause severe, disseminated
or progressive mucocutaneous infections in
immunosuppressed patients.
Adequate treatments that are available for α-herpesvirus
infections include: acyclovir and its oral prodrug
valaciclovir; penciclovir and its oral prodrug famciclovir;
and brivudin (BVDU). BVDU has now been licensed in
several European countries for the treatment of herpes
zoster.Acyclovir and penciclovir are acyclic nucleoside
analogues; in addition, some carbocyclic guanosine
analogues (such as A-5021 and cyclohexenylguanine)
and methylenecyclopropane analogues of nucleosides
(such as synguanol), have been accredited with potent
activity against HSV-1, HSV-2 and VZV9. Some of the
methylenecyclopropane analogues have also proved
effective against β- and γ-herpesviruses and hepatitis B
virus (HBV).
As acyclic nucleoside analogues require phosphorylation
by the virus-encoded thymidine kinase (TK) to
exert their antiviral activity, they do not inhibit
the TK-deficient HSV or VZV strains that can occasionally
arise, particularly in immunocompromised hosts.
In this situation, infections should be treated
with foscarnet, a pyrophosphate analogue, or the
acyclic nucleoside phosphonate cidofovir, neither of
which depend on the HSV or VZV TK for their
antiviral action
Also dependent on the activity of a viral TK, but
specifically the VZV-encoded TK, are the bicyclic
furo(2,3-d)pyrimidine nucleoside analogues (BCNAs)
Cf 1368, Cf 1369, Cf 1743 and Cf 1742. These compounds
inhibit VZV replication at subnanomolar
concentrations and, even at 100,000-fold greater concentrations,
are not toxic to host cells. Unlike the
‘classical’ anti-VZV compounds, the BCNAs are selective
for VZV and are therefore inactive against HSV-1
and HSV-2. The alkyl(phenyl) side chain on the furanyl
ring of the BCNAs is an important determinant of the
specificity of these compounds14. New anti-HSV agents
that target the viral helicase–primase complex15 — the thiazolylphenyl
derivatives BILS 179BS and BAY 57-1293 — were
recently reported to have in vivo efficacy in animal
models of HSV-1 and HSV-2 infection. These compounds
seem to function by enhancing the affinity of
the helicase–primase complex for the HSV DNA. This
complex comprises three viral proteins — the HSV
UL5, UL8 and UL52 gene products— which
together unwind the double-stranded viral DNA and
generate primers for DNA synthesis by the viral DNA
polymerase. The antiviral potency of BAY 57-1293 is
reported to be superior to all compounds that are currently
used to treat HSV infections.These data validate
the further pursuit of helicase–primase inhibitors for the
treatment of HSV infections.
ANTIVIRALS AND ANTIVIRAL
STRATEGIES Nature Reviews
Erik De Clercq
P.S. Выделенно мной
не пости чушь.