Multiplication of viruses

Viruses can replicate only inside a host cell, exploiting its metabolic apparatus and using its own genetic information; however, multiplication occurs only in cells susceptible to the virus, that is, provided with specific surface receptors and capable of carrying out the replicative phases of its genome.

The multiplicative process is divided into various phases:

1st phase: attack or adsorption of the virus to the cell membrane;

2nd stage: penetration of the virus or its nucleic acid into the cytoplasm of the cell;

3rd phase: undressing or eclipse (loss of viral envelopes and exposure of nucleic acid);

4th phase: replication (synthesis of macromolecules, ie DNA, RNA and viral proteins); viruses have different replicative strategies and each of them multiplies in a different way, exploiting enzymes and organelles of the host cell;

5th phase: assembly (formation inside the cell - in the nucleus or in the cytosol - of the capsid; inside this envelope the viral DNA is inserted, forming the nucleocapsid);

6th phase: release or escape of the virus from the cell.

With some exceptions, the viral replication cycle is very rapid and is completed in 8-24 hours. Each of these phases is complex and typical of each species; in fact, there is a great variety of replicative strategies and mechanisms; the first two (adsorption and penetration) and the last (exit), for example, are different depending on whether the virus has pericapsid or not. While bacteriophages inject their nucleic acids directly into the cytoplasm of the host cell, those animals enter by pinocytosis and are released both by cell lysis and by pinocytosis; during this passage the new virions acquire the phospholipid coat and after leaving they can infect new cells.

Virus attack, penetration and replication

Naked viruses enter the cell by micropinocytosis, also called viropepsis, that is, with the same biological mechanism that it uses to internalize corpuscular substances below 1 μm. Once in the cytoplasm, cell proteases digest the capsid, and nucleic acid (viral DNA) is released into the cytoplasm.

The attack of the virus on the cell is mediated by proteins called antireceptors, present on the viral capsid and on the viral pericapsid, which recognize molecules or proteins present on the cell surface and called receptors. The adsorption phase is therefore mediated by the interaction between antireceptor and receptor.

ADSORPTION: stereochemical interaction between specific chemical groups exposed on the external surface of the susceptible cell (receptors) and of the virion (antireceptors).

HIV, for example, attacks mainly T helper lymphocytes, because it has antireceptors that recognize specific proteins exposed on their cell surface. The antireceptor of the HIV virus is a pericapsid glycoprotein, called GP120, while that of the T lymphocyte is called CD- 4; for this reason the T helper lymphocyte is also known as T4. Once bound, the virus can enter the cell in two ways:

fusion from outside: the pericapsid fuses with the cell membrane and is released into the cytoplasm (typical of HIV and coated viruses);

fusion from the inside: the virus enters a vesicle by pinocytosis. Once in the cytoplasm, the pericapsid merges with the vesicle membrane and the capsid is released into the cytoplasm, as happens for example to the influenza virus and in general to naked ones.

As anticipated, there are many variations in the way the virus enters the host cell.

REPLICATION: viruses have different replicative strategies, conditioned by the type of nucleic acid contained in the capsid; During replication, in general, viruses produce two types of proteins: early (of an enzymatic and regulatory nature, such as polymerases) and late (structural, which will form capsid and pericapsid). In any case, replication implies first of all an "alteration and redirection of the metabolism of the host", which allows the virus to multiply its own genome.

The last stage is the exit of the new viruses from the cell (which follows the assembly of the capsid in the nucleus or in the cytoplasm). In general, naked viruses come out by cell lysis; in those coated, however, some viral proteins during replication , responsible for the formation of the pericapsid, go to insert themselves on one of the membranes of the host cell (for example the cytoplasmic membrane, the nuclear one, or the Golgi membrane or the endoplasmic reticulum); in this way, after self-assembly, the nucleocapsid is approaches the modified membrane, the budding process begins and the virus escapes wrapping itself in part in the modified membrane and acquiring the pericapsid (or envelope).

VIRUS-CELL INTERACTION MECHANISMS: viral infection.

PRODUCTION INFECTION: produces new viruses (viral progeny);

RESTRICTIVE: the virus multiplies only when the cell is in certain conditions (for example in phase S);

ABORTIVE: the virus does not replicate but expresses only some proteins without being able to give rise to new virions;

PERSISTENT: it can be chronic - the virus replicates slowly and the cell releases the virus for long periods (months or even years), as in the case of HIV and chronic hepatitis - or latent (the virus genome remains silent in the nucleus of the host cell for long periods, only to be reactivated to give a productive infection, as in the case of herpes simplex or zoster).

TRANSFORMING: typical of oncogenic viruses, which do not kill the cell but transform it in a neoplastic sense. In these cases the viral genome integrates into the cellular one and takes the name of provirus; this alteration can lead to a genetic change of the host cell, which transforms in a neoplastic sense and, by proliferating in an uncontrolled way, transmits the anomalies to the daughter cells.

Viral infection can cause acute illness with a short course and uncomplicated recovery (usually due to a productive infection, as in the case of the common cold), or chronic illness.