Exosomes originate in different cells that contain specific proteins. For example, exosomes released by virus-infected cells contain viral protein particles associated with virus transmission. Viruses, in particular retroviruses, resemble exosomes in terms of size, composition, and function. Exosomes vary between 30 and 150 nm in diameter.
This is a size range similar to that of viruses that range from 25 to 250 nm, with retroviruses that range from 100 to 200 nm. Exosomes affect the viral infection process in two ways, since they modify their content and the body's immune status. On the one hand, it promotes the replication, transmission and infection of the virus and downregulates antiviral immunity. On the other hand, it limits virus infection and enhances antiviral immunity. Based on these two directions, we will summarize the “love and hate” between exosomes and the following viral infections.
As is commonly believed, most viruses can leave host cells in the form of individual particles and be transmitted to uninfected cells. New data have revealed that block viral transmission is transmitted in the form of particles covered with a lipid bilayer through extracellular vesicles, especially exosomes (Exo). The support membrane can originate in multivesicular bodies during the formation of intraluminal vesicles and the autophagic response. Exo are nanometer-sized particles, ranging from 40 to 200 nm, with the ability to harbor various types of signaling molecules from donor cells to recipient cells in a paracrine form, resulting in the modulation of specific signaling reactions in target cells.
The phenomenon of exobiogenesis consists of multiple and complex biological stages involving diverse molecular components and pathways. Because of the similarities between exogenous biogenesis and virus replication and the existence of shared pathways, it is believed that viruses can hijack the biogenesis machinery of exogenous viruses to spread and evade immune cells. To do this, Exos can transmit complete virions (as individual units or aggregates), independent viral components and pure genetic material. This review article aims to analyze the challenges and opportunities related to exosomal virus administration in terms of viral infections and public health.
Exosomes are extracellular vesicles that facilitate intercellular communication and are essential in post-transcriptional regulation within cellular gene regulatory networks, which affects the dynamics of pathogens. These vesicles act as crucial regulators of immune responses, as they mediate cellular interactions and allow the introduction of viral pathogenic regions into host cells. The exosomes released by virus-infected cells harbor various microRNAs (miRNAs), which can be transferred to recipient cells, which modulates virus infection. This transfer is a critical element in exosome-mediated molecular interaction.
In addition, the endosomal classification complex required for transport (ESCRT) within exosomes plays a vital role in virus infection, as components of the ESCRT bind to viral proteins to facilitate virus budding. This review clarifies the role of exosomes and their components in the invasion of viruses into host cells, with the objective of shedding new light on the regulation of viral transmission through exosomes. HIV is the first RNA virus used for exosome research, and it is also one of the most studied viruses. Exosomes and viruses can also be purified using chromatography techniques based on size, affinity, hydrophobicity, or other characteristics.
In the following steps, VP4 is located in the microdomains of the Trans-Golgi apparatus of the lipid raft, leading to the assembly of the rotavirus capsid. Rhinovirus infection is associated with necrosis of airway epithelial cells and inflammation caused by interleukin-1 in young children with cystic fibrosis. The HCV envelope glycoprotein E2 not only exists on the surface of the virus, but can also be released through the exosome pathway. These exosomes can help spread the virus, modulate the immune system, and promote disease progression.
However, affinity-based purification, which uses antibodies that specifically bind to cell surface proteins that vary between exosomes and viruses, can discriminate between them and is used to isolate specific populations of exosomes. The role of viral RNA and co-opted cellular ESCRT-I and ESCRT-III factors in the formation of the tombusvirus spherules that harbor the tombusvirus replicase. In addition, one of the fundamental receptors used by the influenza virus to bind to the target cell is sialic acid, related to amino acids a2,3 and a2.6, which are expressed through exosomes released into the pathways respiratory. These viruses can cause respiratory problems in different ways; for example, they can transfer their DNA or RNA to exosomes.
Based on microfluidic tracing analysis, it has been shown that the number of vesicles containing rotavirus and the amount of vesicle proteins increased after rotavirus infection. PI3-K, through the activation of CCbL (E3ubiquitin ligase), multiubiquitylates EGFR, which drives phosphorylation and ubiquitination of the receptor, and then translocates the receptors bound to the virus into a lipid raft. Hepatitis C virus-induced exosomal microRNAs and Toll-like receptor 7 polymorphism regulate the activation factor of B cells. Stochastic model of acidification, hemagglutinin activation and escape of influenza viruses from an endosome.
Tsg101 is recruited by a late domain of the nucleocapsid protein to promote the formation of particles similar to Marburg virus.
