Chapter 6
• Know the Key Terms (Matching questions). Pg. 93
! AIDS – The later stage of HIV disease that causes a breakdown in the
immune system, leaving the patient unable to fight infection.
! Antiretroviral – Drugs that are a subset of antiviral drugs and specifically
suppress the reproduction of retroviruses.
! Antiviral – Drugs capable of interfering with the ability of the virus to carry
out its reproductive functions.
! cART – A combination of antiretroviral drugs that must be taken every day
to combat the progression of HIV disease from becoming AIDS or to prevent
HIV infection after exposure.
! Entry Inhibitor – Antiretroviral drugs that prevent cellular infection with
HIV by blocking the CCR5 receptor on CD4+ T cells.
! Fusion Inhibitor - Antiretroviral drugs that prevent cellular infection with
HIV by clocking the ability of HIV’s surface protein gp41 to fuse with the
host cell’s CD4 receptor.
! HIV – The specific retrovirus responsible for the immune system problems
associated with destruction of helper T cells (CD4 cells) when the infection
results in HIV disease and progresses to AIDS.
! Integrase Inhibitor – Antiretroviral drugs that inhibit the HIV enzyme
integrase, which the virus uses to insert the viral DNA into host cell’s
human DNA.
! Non-Nucleoside Reverse Transcriptase Inhibitor (NNRTI) – Antiretroviral
drugs that work by binding directly to the HIV-1 enzyme reverse
transcriptase, preventing viral cells DNA replication, RNA replication, and
protein synthesis.
! Nucleoside Reverse Transcriptase Inhibitor (NRTI) – Antiviral drugs that
have a similar structure to the four nucleoside bases of DNR, making them
“counterfeit” bases. When these counterfeit bases are used by the HIV
enzyme reverse transcriptase, viral DNA synthesis and reproduction are
suppressed.
! Opportunistic Infection – a virus, bacteria, protozoa, or fungi that takes
the “opportunity” to cause an infection in an immunocompromised host.
! Protease Inhibitor (PI) – Antiretroviral drugs that suppress the formation
of infectious virions by inhibiting the retroviral protease enzyme.
! Retrovirus – Viral organisms that carry special enzymes (reverse
transcriptase, integrase, and protease) with them and use RNA (ribonucleic
acid) instead of DNA (deoxyribonucleic acid) as their genes to reproduce.
! Virion – New viral particles reproduced in cells infected with retroviruses
that can leave the cell and infect more human body cells.
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! Virus – A small infectious agent that can reproduce only inside other living
cells, including human cells.
• Know the Key Points (True/False questions). Pg. 104
• Know the difference between Virucidal and Virustatic. Pg. 94
Antivirals Does not kill virus, but stops viral reproduction; virustatic
(hinders virus), not virucidal (kills virus). Operates in a variety of ways.
•
• Study Table 6.1 on Pg. 95. Know the routes of administration for the
drugs on that table (Orally, Inhalation, Intravenous, Topical).
Oseltamivir- orally (Nueraminadase inhibitor )
Zanamivir - inhalation ( NI)
Acyclovir - IV (Viral DNA PI)
Penciclovir - topical (Viral DNA PI)
Amantadine , Rimantadine - orally (Uncoating inhibitors
• Know the medications in Table 6.1 on Pg. 95. Know what class is given
for influenza and HSV.
• Influenza- Neuraminadase inhibitors (oseltamivir Relenza , zanamivir
Tamiflu)
Uncoating Inhibitors ( amantadine Symmetrel, rimantadine
Flumadine )
HSV medications
Viral DNA Polymerase Inhibitors acyclovir (Zovirax)
(-vir) - have shown that high doses of
favipiravir were able to prevent famciclovir (Famvir)
human cells from being infected with penciclovir (Denavir)
SARS-CoV-2.
valacyclovir (Valtrex)
• What classification of antivirals are given for Influenza and to prevent
initial infection? Pg. 94-95
Uncoating Inhibitors (-dine) – Prevents initial influenza infection and spread of
influenza infection by interfering with viral uncoating, which is needed for viral
fusion with host cells, the first step of cellular infection.
amantadine (Symmetrel)
rimantadine (Flumadine)
• Antivirals work best when given within the 48 hours of onset of symptoms
Pg. 94