I am not a specialist virologist, so this is slightly outwith my field. However if you are going to learn a bit about viral replication then you should go no further than HIV. It is probably the most interesting.

The beauty about the HIV replication cycle is that each major step can now be complemented with an HIV anti-viral drug. (almost certainly due to the massive amount of research done on HIV.)

There are six main steps to HIV replication, described in the bullets and the diagram below. (This is fairly basic and can be expanded upon considerably depending upon how much detail you need to know the topic)

1) Attachment:- HIV virus attaches to receptors (usually CCR5 but occasionally CXCR4 or other receptors) on macrophages or CD4 Lymphocytes.

2) Fusion:-Fusion between gp120 on the virion and CD4.

3) Reverse Transcription: The reverse transcriptase enzyme converts the HIV RNA strand into a DNA. The reverse transcriptase enzyme also has DNA dependent DNA polymerase activity which create a complementary DNA strand. The double stranded DNA is then transported to the cell nucleus.

4) Integration: The HIV dsDNA is incorporated into the host cell nucleus.

5) Replication: During viral replication the HIV proviral DNA is converted into mRNA (transcription). Some of this mRNA is converted into regulatory proteins tat and rev and into structural proteins such as gag and env.

6) Assembly: During this stage, the HIV polyproteins are converted/cleaved into functional HIV proteins by proteases, and the virion assembles on the inner surface of the plasma membrane through gag proteins and starts to bud from the cell wall.

 

Antiretroviral (ARV) drugs are broadly classified by the phase of the retrovirus life-cycle that the drug inhibits.

• CCR5 receptor antagonists are the first antiretroviral drugs which do not target the virus directly. Instead, they bind to the CCR5 receptor on the surface of the T-Cell and block viral attachment to the cell. Most strains of HIV attach to T-Cells using the CCR5 receptor. If HIV cannot attach to the cell, it cannot gain entry to replicate. e.g. maraviroc
• Fusion inhibitors interfere with binding, fusion and entry of HIV-1 to the host cell by blocking one of several targets. e.g. enfuvirtide
• Nucleoside reverse transcriptase inhibitors (NRTI) and nucleotide reverse transciptase inhibitors (NtRTI) are nucleoside and nucleotide analogues which inhibit reverse transcription by being incorporated into the newly synthesized viral DNA strand as faulty nucleotides; they both act as competitive substrate inhibitors. e.g. zidovudine (AZT), lamivudine (3TC)
• Non-Nucleoside reverse transcriptase inhibitors (NNRTI) inhibit reverse transcriptase by binding to an allosteric site of the enzyme; NNRTIs act as non-competitive inhibitors of reverse transcriptase. e.g. efavirenz, nevaripine.
• Integrase inhibitors inhibit the enzyme integrase, which is responsible for integration of viral DNA into the DNA of the infected cell. e.g. raltegravir
• Protease inhibitors (PIs) target viral assembly by inhibiting the activity of protease, an enzyme used by HIV to cleave nascent proteins for the final assembly of new virions. e.g. ritonavir, nelfnavir.
• Maturation inhibitors inhibit the last step in gag processing in which the viral capsid polyprotein is cleaved, thereby blocking the conversion of the polyprotein into the mature capsid protein (p24). Because these viral particles have a defective core, the virions released consist mainly of non-infectious particles. e.g. alpha interferon

 If you were to learn the replication cycles of any other viruses, then the next two I would go for are Hepatitis B and Influenza.