Parvovirus B19

P-B19

Morphology

Parvovirus is a nude virus type with DNAss(single strand) that can has both polarities, aproximately 50% (+) and 50% (-). The virus can resist a long range of Ph (3-9) and 60 minutes at 56ºC. Core is composed by VP1, VP2 and VP3, the structural proteins creating an icosaedric core with aproximately 12-32 capsomers. VP2 encompasses 80% virion mass. NS1 is functional protein necessary for replication. It can be inactivated by formalin.

Replication

The virus tropism is for replicating cells (going through S or G1 phase) because he is incapable of doing it. The virus doesn't count with the machinary for replication, so, needs host cell enzymes. The B-19 can stablish two types of infection permissive persistent and non permissive persistent. The first group of cells is composed by erythroblasts and erythroid progenitors (from bone marrow and fetal liver); the second group is composed by hepatic cells, endothelium, megacariocytes, BC, TC, mast-cells, Macrophages, epithelium and sinovium cells, fetal liver cells, fetal heart cells and placenta. The permissive kind allows the virus to destroy the cell and release virions. the non permissive kind go through apoptosis and stops viral spread.


Initially, the virus links this kind of cells via P antigen (globoside) and goes to the nucleus and is transcrypted and spliced, then RNAm is translocated to endoplasmic reticulum for protein synthesis. All of this come back to the nucleus, where VP1, VP2 and VP3 become the core and NS1 allow the DNA replication and core packing, this new virion can be (+) or (-) polarity. Last, if the cell is permissive there are cell lysis and virion release, if don't, the cell goes through apoptosis.

Pathology Spectrum

The pathology is up to the infected person. In pregnant womans, can be described in two ways: infectious erythema and hydrops fetalis.
In inmunodeficient patients can appears as pure red cell aplasia and transient aplastic crisis.
In inmunocompetent patients can appear like infectious erythema, arhtritis, SEL, sholein-henoch purpura, encephalitys.

Viral pathogenesis

In permissive cell there are lysis, in non permissive cells there are cytotoxicity because of NS1, in erythroblasts there are apoptosis because of NS1, ann lastly in all of them there are chronic inflamatory response.

Inmunopathogenesis

• Anti-body production of IgG-VP1 that can have cross reaction against type II colagen and queratine.
• Antibody production against viral antigens and deposit.
• NS1 can elicit in endothelium, IL-6 release that stimulate BC to proliferate in a polyclonal way.

Laboratory

At the week of current infection, there are Ig-M, later, after the second week there are IgG that stay elevated very long time. About symptoms: at the week of curret infection there are fever, headache, malaise. In the 2-3º week there are RASH and anthralgias.