life cycle and antiviral effect by uzair hashmi n.
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life cycle and antiviral effect By uzair hashmi. Major steps . Recognition Attachment Penetration Uncoating Early protein synthesis Nucleic acid synthesis Late protein synthesis Assembly Release. Attachment/Adsorption.

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major steps
Major steps
  • Recognition
  • Attachment
  • Penetration
  • Uncoating
  • Early protein synthesis
  • Nucleic acid synthesis
  • Late protein synthesis
  • Assembly
  • Release
attachment adsorption
  • Virus attachment is through temperature independent ionic interaction
  • VAPs recognize specific receptors on the cell surface
  • Cells without the appropriate receptors are not susceptible to the virus.

An energy-dependent process, and the cell must be metabolically active for the penettration

  • Three main mechanisms are involved:

1)Translocation of the entire virus particle across the plasma membrane.

2) Endocytosis of the virus into intracellular vesicles (endosomes).

3) Fusion of the virus envelope with a cellular membrane.

  • Uncoating is a process that viral capsid is degraded by viral enzymes or host enzymes
  • Some examples of uncoating
    • Direct uncoating: paramyxoviridae
    • Partial uncoating: Hiv
    • Endosomal fusion: influenza virus
    • Endosomallysis: adenovirus
replication synthesis
  • Replication involves assembly of viral proteins and genetic materials produced in the host cell.
  • begins immediately after the process of uncoating. The synthesis stage leads to the massive production of viral components.
  • involves transcription and the use of host ribosome to translate the viral mRNA into viral proteins. However, the strategies employed are different for different viruses.
replication synthesis1

The important strategies in the synthesis of various viral genome syntheses are :

  • dsDNA(+/-) Class I
  • ssDNA(+) dsDNA intermediate Class II
  • dsRNA(+/-) Class III
  • ssRNA(+) class IV
  • ssRNA(-) class V
  • ssRNA(+) DNA intermediate class VI
  • dsDNA (+/-) RNA intermediate class VII
  • The last stage of virus replication cycle. Thousands of newly formed virus progeny leave the host cell in search of a new host cell, thus establishing an infection in the body.

Release includes:

  • Lysis
  • Budding
    • At the plasma membrane
      • HIV assembly
      • Influenza assembly
    • At membrane of the cell organelles like endoplasmic reticulum (ER) or golgi apparatus
    • Synthesis and glycosylation of envelope proteins
  • Cell-cell fusion
viral attachment n entry


  • works by disrupting the HIV-1 molecular machinery at final stage of fusion with target cell, preventing uninfected cells from becoming infected. Mimics components of the HIV-1 fusion machinery and displaces them, preventing normal fusion.
  • maraviroc(HIV): an entry inhibitor,blocks gp120 (V3 loop), which normally associates with the chemokine receptor CCR5. HIV is then unable to bind and enter human macrophages. Because HIV can also use another coreceptor, CXCR4, an HIV tropism test such as a trofile assay must be performed to determine if the drug will be effective.


  • by inhibiting the fusion of the human host cell with the viral envelope of the herpes virus, thus preventing its replication. This mechanism has neither been directly observed nor proven, however.

Interferon alpha:

  • produced by leukocytes.
  • involved in innate immune response against viral infection.
  • come in 14 subtypes that are called IFNA1, IFNA2, IFNA4, IFNA5, IFNA6, IFNA7, IFNA8, IFNA10, IFNA13, IFNA14, IFNA16, IFNA17, IFNA21. genes for these IFN-α molecules are found together in a cluster on chromosome 9.

IFN-α is also made synthetically as medication.

Types are:

  • Pegylated interferon alfa-2a
  • Pegylated interferon alfa-2b
  • Amantadine(influenza):

mechanism of Amantadine's antiviral activity involves interference with a viral protein, M2, required for the viral particle to become "uncoated" once taken inside a cell by endocytosis

  • rimantadine(influenza):

inhibits influenza's viral replication, by preventing the uncoating of the virus's protective shells, the envelope and capsid.

nucleic acid synthesis
  • RTIs(HIV):. RTIs block reverse transcriptase's enzymatic function and prevent completion of synthesis of the double-stranded viral DNA, thus
  • The hepatitis B virus,, employs a RNA-dependent DNA polymerase to replicate. RTIs can also block HBV replication; when used in this way they are referred to as polymerase inhibitors
late protein synthesis and processing
  • protease inhibitors(HIV):

PIs prevent viral replication by inhibiting the activity of proteases, e.g.HIV-1 protease, enzymes used by the viruses to cleave nascent proteins for final assembly of new virons.


neuraminidase inhibitors(influenza)

  • antiviral drugs targeted at the influenza virus,
  • work by blocking the function of the viral neuraminidase protein, thus preventing the virus from reproducing by budding from the host cell.
  • Oseltamivir (Tamiflu) a prodrug, Zanamivir (Relenza) and Peramivir belong to this class. Unlike the M2 inhibitors, which work only against the influenza A, neuraminidase inhibitors act against both influenza A and influenza B.