·Generation of a novel strain due to co-infection of different strains in an individual (random assortment)
Human Factors
·Concentration of people with shared lifestyle
oE.g. the sharing of hypodermic needles, unsafe sex
·Breakdown in public health
oMainly in third world countries
·Climate change
oE.g. increased wet seasons will lead to more stagnant water which might make it more conducive for mosquito breeding in a particular area. Aedes mosquito is a vector of dengue fever. Thus, the spread of the dengue flavivirus will be enhanced.
·The amount of virus is plotted on a logarithmic scale as a function of time after infection.
·At the start, the virus disappears but viral nucleic acid continues to function and begins to accumulate within the cell as the virus is replicating in the cell. The time during which no virus is found inside the cell is known as the eclipse period. The eclipse period ends with the appearance of virus.
·The latent period is defined as the time from the onset of infection to the appearance of virus extracellularly.
·Alterations of cell morphology accompanied by marked derangement of cell function begin toward the end of the latent period.
·At the end of the latent period, new progeny viruses are assembled and released as the cell bursts.
·Infection begins with one virus particle and ends with several hundred virus particles having been produced. This is known as productive infection.
·The virus attachment proteins on the surface of the virion attach to specific receptor proteins on the host cell surface through weak, noncovalent bonding.
·The specificity of attachment determines the host range of the virus.
·Receptor on host cell mediates viral entry into cell.
Routes of Host Entry
·Clathrin coated pits in endocytosis: Naked viruses such as the Hepatitis C virus.
·Receptor-mediated endocytosis: Enveloped viruses such as the Epstein Barr Virus.
·Fusion: Lipid bilayer of virus fuses with lipid bilayer of host cell.
·Direct penetration: Translocation of entire virus particle mediated by receptor.
Uncoating
·The viral genome must be separated from its protein coat once the virus enters the host cell’s cytoplasm. This process is called uncoating.
·Naked viruses are uncoated by proteolytic enzymes from host cells or from the viruses themselves.
·The uncoating of viruses such as the poxviruses is completed by a specific enzyme that is encoded by viral DNA and formed soon after infection.
·Polioviruses begin uncoating even before penetration is complete.
Replication and Expression
·After uncoating has taken place, genome replication and gene expression takes place—mRNA is synthesized, processed and translated to produce viral proteins.
·At this point, viruses follow different pathways depending on the nature of their nucleic acid and the part of the cell in which they replicate.
Assembly
·Assembly depends on the site of synthesis
·Sites of protein synthesis and processing are the endoplasmic reticulum and Golgi body.
·Sites for assembly are the nucleus, endoplasmic reticulum and Golgi body.
·The progeny particles are assembled by packaging the viral nucleic acid within the capsid proteins.
Release
·Virus buds off the plasma membrane of the host cell, and an envelope forms around the new viruses.
oVirus specific proteins enter the cell membrane at specific sites
oThe viral nucelocapsid then interacts with the specific membrane site mediated by the matrix protein.
oThe cell membrane evaginates at that site, and an enveloped particle buds off from the membrane.
oThis usually occurs with enveloped viruses. An exception is the herpesviridae family, whose members acquire their envelopes from the nuclear membrane rather than the outer cell plasma membrane.
·Alternatively, there may be an accumulation of particles in vesicles and release via exocytosis. This usually occurs with enveloped viruses.
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