It is commonly accepted that the spread of most viruses occurs via the diffusion of ‘cell-free’ viral particles. In support of this, infectious viruses have been found in biological fluids and aerosols, and could be propagated in vitro using virus stocks produced from infected cell-culture supernatants. This mode of viral dissemination requires high numbers of stable viral particles released by the infected cell into the extracellular environment, such as the host bodily fluids. ‘Free’ viral particles were associated with a variety of components, such as lipids or proteins, which might reinforce virus envelop integrity and prevent envelope glycoprotein shedding. However, for other viruses, few viral particles are released, or they are poorly infectious when separated from infected cells. In such cases, virus propagation largely requires the presence of infected cells, suggesting that cell contacts mediate viral spread. This type of dissemination is mainly reported for enveloped viruses, such as some herpes viruses and some retroviruses, particularly deltaretroviruses such as the human T-cell leukemia virus type 1 (HTLV-1). Many aspects of this mode of virus dissemination are largely unknown, such as (i) the nature and the mechanism for forming cellular junctions that mediate cell–cell virus spread, and (ii) the nature of the infectious material transferred. Both of these factors depend on the virus and the type of infected cells.
Of note, the spread of two human retroviruses that infect leukocytes, HIV-1 and HTLV-1, occurs between mobile cells forming dynamic contacts with other cells. Both retroviruses cause severe chronic viral infections. Their transmission between individuals occurs through sexual contact and blood transfusion, and vertically from mother to child, including through breastfeeding. In addition to HTLV-1 dissemination through division of infected cells carrying viral genomes, transmission of HTLV-1 viral particles is known to occur mainly through cell contact in vitro and in vivo, with the exception of dendritic cells, which can be infected by cell-free viral particles. By contrast, HIV-1 spread can occur by both diffusion and direct cell–cell transfer. Nevertheless, compelling evidence indicates that direct spread through cell contact is the most efficient mode of HIV-1 dissemination in vitro, and might play a crucial role in vivo:
Can viruses form biofilms? Trends Microbiol. Mar 31 2011
The recent finding that the human T-cell leukemia virus type 1 (HTLV-1) encases itself in a carbohydrate-rich adhesive extracellular ‘cocoon’, which enables its efficient and protected transfer between cells, unveiled a new infectious entity and a novel mechanism of viral transmission. These HTLV-1 structures are observed at the surface of T cells from HTLV-1-infected patients and are reminiscent of bacterial biofilms. The virus controls the synthesis of the matrix, which surrounds the virions and attaches them to the T cell surface. 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.