With new evidence emerging that viral latent infections might have yet unknown negative effects, it is becoming a necessity to look into the factors that allow these viruses to persist and establish latency. Designing vaccines that will prevent the initial infection and establishment of latency should become the main focus. To succeed in such a goal is not impossible but requires major refocusing of the research efforts. The viral escape mechanisms that are used during the initial stages of the acute primary infection should be carefully examined and fully understood. Once this is accomplished, developing strategies that will disarm these escape mechanisms and allow the immune system to clear the virus should become an achievable goal.
Keywords: EBV, VZV, HIV, CMV, HSV-1, HSV-2, viral latency, persistent viral infection, chronic viral infection, reactivation, mucosa, herpesviridae, herpes zoster, varicella, Varivax®, Zostavax®, retroviruses, gp350, gp220, gp85 (gH), gp25 (gL), gp42/38, CR2, CD21, C3, C3d, C3b, C3a, C3c, iC3b, C5a, C3dg, C3d, gB, gC, gD, gE, gG, gH, gI, gJ, gK, gL, gM, gH-gL, gM-gN, heparan sulphate, lectin pathway, IgA, IgG Fc, DC-SIGN, Trojan horse, CCR5, CXCR4, TGF, regulatory T cells, virokines, viroceptors, CD103+ DCs, DAF, MCP, amplification loop, complement