Een besmetting met Epstein-Barr-virus (EBV) wordt nooit geheel opgeruimd. Zoals bij alle herpesvirussen blijft er een latente infectie over. Daarnaast is het EBV-genoom op een speciale manier latent aanwezig in B-lymfocyten. Aangetoond is dat volwassenen af en toe virus in het speeksel uitscheiden. Bij onderdrukking van het afweersysteem stijgt het aantal uitscheiders van 20 tot 50.2
Worldwide, four in five adults are infected with herpes simplex virus (HSV), say researchers. But most of those infected don’t show symptoms like cold sores because the virus infection is “latent” or “silent” — sleeping — within the nervous system, where it remains for the entire life of its host.
The herpesvirus that causes these two illnesses actually remains inside your nerve cells for a lifetime. They’re able to do it because your immune system can’t reach them there. Indeed, viruses generally hide by exploiting blind spots in the immune system. That means generally one of two things: 1) infecting areas of the body that aren’t entirely under the control of our immune systems or 2) going dormant inside cells so that the immune system can’t detect them.
Viruses stay hidden in our bodies by exploiting a vulnerability in our immune systems. This vulnerability is called “immune privilege,” and comes from an old observation that foreign tissue transplanted into certain parts of the body don’t elicit the usual immune response. This includes the brain, spinal cord, and eyes. Scientists believe this is because the brain, spinal cord, and eyes are simply too delicate and important to withstand the inflammation that’s typical of an immune response.
As your immune system beats back VZV, the virus retreats inside your nerve cells. There, they stop hijacking the cell’s molecular machinery and they stop reproducing. Those segments of viral DNA just hang out, lying low until some trigger awakens them. Usually the trigger is some kind of stress or health disturbance. That’s when VZV mounts it attack again, spreading along nerves and causing the characteristic streaks of itchy rashes in shingles.
VZV is in the family of herpesvirus, which all have the ability to lie dormant in cells. Herpesvirus include, yes, herpes simplex virus types 1 and 2, which cause cold sores and genital herpes, but also Epstein-Barr and cytomegalovirus, which cause mono. In the case of the herpes simplex viruses, scientist have found that certain genes, called latency associated transcript (LAT), are most active when the virus is dormant. The LAT blocks the expression of genes used when the virus is active.
Another mode of virus infection is the latent phase, where the virus is ‘quiescent’ (a state in which the virus is not replicating). A combination of these stages, where virus replication involves stages of both silent and productive infection without rapidly killing or even producing excessive damage to the host cells, falls under the umbrella of a persistent infection. Reactivation is the process by which a latent virus switches to a lytic phase of replication. Reactivation may be provoked by a combination of external and/or internal cellular stimuli.
The focus of the article is on those viruses known to cause latent infections, which include herpes simplex virus, varicella zoster virus, Epstein–Barr virus, human cytomegalovirus, human herpesvirus 6, human herpesvirus 7, Kaposi’s sarcoma-associated herpesvirus, JC virus, BK virus, parvovirus and adenovirus.
The ability to move back and forth from latent to lytic infections helps the virus spread from infected individuals to uninfected individuals. Apart from these two phases, a few viruses also have yet another method of replication, termed ‘persistent infection’. Persistent viruses (e.g., hepatitis B virus) are those that are not eliminated following primary infection and remain in specific cells of the infected individuals. An infected individual experiences a persistent infection in which the virus is capable of replicating slowly, silently or at low levels without causing excessive damage to the host cell.
Viral reactivation is associated with several stress factors [1], including viral infection (with other viruses), nerve trauma, physiologic and physical changes (e.g., fever, menstruation and exposure to sunlight) and immunosuppression (as in cytomegalovirus [CMV] disease)
Viruses that infect the nervous system may cause acute, chronic or latent infections.
Persistent infections are characterized as those in which the virus is not cleared but remains in specific cells of infected individuals. Persistent infections may involve stages of both silent and productive infection without rapidly killing or even producing excessive damage of the host cells. There are three types of overlapping persistent virus-host interaction that may be defined as latent, chronic and slow infection.
Pathogenesis
The mechanisms by which persistent infections are maintained involve both modulation of virus and cellular gene expression and modification of the host immune response. Reactivation of a latent infection may be triggered by various stimuli, including changes in cell physiology, superinfection by another virus, and physical stress or trauma. Host immunosuppression is often associated with reactivation of a number of persistent virus infections.
We propose that, similar to bacterial biofilms, viral biofilms could represent 'viral communities' with enhanced infectious capacity and improved spread compared with 'free' viral particles, and might constitute a key reservoir for chronic infections.
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