D.7 Antivirals

D.7.1 State how viruses differ from bacteria.
Viruses - HIV virus with lipid envelope
- lipid envelope
- viral proteins incorporated in envelope
- viral RNA
- core protein
- 25 nm

Bacteria - T4 bacteriophage
- DNA
- protein coat
- sheath
- base plate
- tail fibre
- 98nm

Viruses (e.g. measles, meningitis, polio, AIDs, avian flu)
- contain only 2 components: protein & nucleic acid (RNA or DNA)
- no cellular structure
- only produce inside another living cell
- original hijacker: take over functioning of host cell & use to reproduce, host cell used to assemble new viral particles & in the process the host cell usually dies,  therefore thousands of viral particles are released into the body.

Bacteria
- more complex cellular structure
- survives & reproduces independently


D.7.2 Describe the different ways in which antiviral drugs work.
Mutation: small changes in genetic material

Viruses
- live in cells, therefore can't be easily targeted
- lack bacteria cell structure, therefore not attacked by antibiotics
- speedily multiple, therefore often already spread through the body before symptoms appear
- have a tendency to mutate rapidly, therefore change is susceptible to drugs
e.g. different flu vaccines developed each year according to most abundant strain of cirus

Antibodies
Antivirals - alter cell's DNA, therefore virus can't use to multiply
or - block enzyme activity within host cell, therefore prevents virus reproduction then, relief from symptoms & disease progression halted, but not completely eradicated from the body (e.g. flare-up: herpes infection, cold sores)

Amantadine 
- an effective antiviral drug
- changes cell membrane, therefore prevents virus entry into cells.
- best used as prophylactic (preventive) treatment, or before infection spreads widely.
- effectively used to treat influenza


D.7.3 Discuss the difficulties associated with solving the AIDS problem.
HIV
- primarily infects vital white blood cells (CD4+T cells) in immune system
- binds to specific receptor proteins on cell surface then penetrates cell
- is a retrovirus (has RNA instead of DNA); RNA released into cell & enzyme reverse transcriptase controls synthesis of viral DNA from RNA. Viral DNA integrates itself into host cell's DNA, therefore when the cell divides the viral DNA is also replicated.

Process:
1. HIV destroys T-helper cells (cells that defend the body against the virus)
2. HIV mutates very rapidly even within a patient (estimated there are more variations of HIV in a single patient than influenza world wide in a year)
Variation: virus 'escapes' immune response, because patient has to develop a new response to the newly mutated virus.
3. HIV often lies dormant in host cells, therefore immune system has nothing to respond to.


AIDs - caused by HIV
- the failure of the immune system, therefore the body falls prey to pneumonia/cancers (~40 million are HIV positive, they have a likelyhood of developing AIDs)


Antiretroviral drugs
- helps fight against HIV at different stages of HIV lifecycle
- targets to inhibit enzyme reverse transcriptase, b/c its specific to virus & doesn't affect host cell.

Zidovudine (AZT)
- effectively delays disease progression
- used to prevent mother-to-child transmission of HIV during pregnancy

Other antiretrovirals 
- blocks HIV binding to cell membranes
- or inhibits assembly of new viral particles in cells

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Unpleasant to serious side effects, but successful in helping prolong length & quality of life of HIV infected.

Vaccine for HIV/AIDs failed so far, because variable virus nature & immune response acts too slowly in the case of HIV infection.

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