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The Viruses
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Many factors determine susceptibility of cells to viral infection and the resultant pathology. However, the outcome of viral infections in terms of host survival is often governed by the host immune response to antigenic viral proteins (Figure 16.3). Much of the pathology of viral diseases may be due to chronic inflammation in infected tissues and to immunopathologic effects associated with the response of the immune system to infection of cells. Many viruses become latent after infection and produce few if any viral transcripts or viral proteins. Viral latency may be a part of the natural life cycle of the virus or may be imposed on the virus as a result of the host′s immune response (Figure 16.4). Latency allows the viral genome to persist in a quiescent or inactive state in the host. Periodic activation may lead to the development of recurrent disease. Reactivation of the genome and production of new virus may contribute to cellular transformation and the development of malignancies. In persistent infections in which a viral genome is relatively limited in expression, the host cell may express few viral antigens and is less susceptible to immune attack. However, in some persistent infections active viral antigen production occurs and such infections may result in tissue injury from the deposition
Progressive multifocal leukoencephalopathy
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Eric M. L. Williamson, Joseph R. Berger
Though it is hypothesized that there is no evidence for any biological activity for the archetype sequence or virus isolates, there have been patients with PML in whom CSF samples have identified virus that contain these sequences—so even if spread is from kidney to the brain, both viruses are capable of neuroinvasion. At the same time, several regulatory region sequences have been identified from JCV DNA in peripheral blood of PML patients that are not related to the archetype but closely related to sequences found in PML brain [71]—the latter lending credence to theories that the virus mutates in the periphery. Additional sites of viral latency have been reported through pathology studies, including detection of archetype virus in a variety of tissues [90]. Further examination of the distribution and importance of the archetype sequence is needed to understand its role in the pathogenesis of PML.
Control of Herpesvirus Infections
Published in Fred Rapp, Oncogenic Herpesviruses, 2019
In this chapter a number of treatments and attempts at prevention of human herpesvirus infections will be discussed. Some of the treatments reflect the state of the art and are employed in clinical situations; others are experimental. While this volume is primarily concerned with herpesvirus oncogenesis, discussion of treatment and control of herpesvirus infections must largely pertain to in vivo infections where induction of neoplasms is not necessarily an issue, e.g., HSV encephalitis. Inhibition of herpesvirus replication that is limited to experimental in vitro systems will not be discussed. Prior to evaluation of herpesvirus control and treatment, the natural history of infection by human herpesviruses will be outlined. Because of the role of virus “latency” in herpesvirus infections and the importance of latency in planning antiviral treatment, latency will also be briefly discussed (see also Volume II, Chapter 1).
Emerging therapeutic targets for nasopharyngeal carcinoma: opportunities and challenges
Published in Expert Opinion on Therapeutic Targets, 2020
Valentin Baloche, François-Régis Ferrand, Anna Makowska, Caroline Even, Udo Kontny, Pierre Busson
Like for all herpesviridae, production of EBV viral particles results ipso facto in the death of the infected cell, hence the name of lytic cycle to characterize a state of infection oriented toward production of viral particles. The idea of disrupting viral latency in EBV-positive malignant cells has been in the air for decades (for a review see Oker et al., Intechopen.com, DOI: 10.5772/64738). Initially the idea was to use EBV as a kind of endogenous oncolytic virus but this was not realistic for at least 2 reasons. First, the mechanisms blocking the lytic cycle operate at multiple levels and it is much easier to obtain partial activation of several lytic genes than to achieve viral production in all cells. Next, activation of the lytic cycle is known to favor the release of soluble factors, especially cytokines, with potential oncogenic activity on bystander cells. Therefore, most investigators in the field aim to partial activation of lytic genes in order to induce expression of viral enzymes with the capacity to transform prodrugs in cytotoxic drugs, specifically in malignant cells. The two main candidate enzymes for this function are EBV thymidine kinase (EBV-TK) and EBV protein-kinase (EBV-PK). Another aim of partial lytic induction could be to increase the immunogenicity of malignant cells.
Novel therapeutic approaches for targeting TB and HIV reservoirs prevailing in lungs
Published in Expert Opinion on Drug Delivery, 2019
Mrunal Jadhav, Tabassum Khan, Chintan Bhavsar, Munira Momin, Abdelwahab Omri
CD4+ T cells are the primary targets of HIV; however, HIV also integrates itself in macrophages and dendritic cells. Existence of enriched HIV reservoirs in CNS, gut-associated lymphoid tissue (GALT), genitourinary (GU) tract, and lungs is debatable albeit of much importance [7,8]. Interestingly, the viral load in these reservoirs varies based on age, highly active antiretroviral therapy (HAART) duration, gender, and viral subtype. The contribution of these reservoirs to viral latency remains elusive [8]. And thus, eradication of HIV from these reservoirs is debatable as the current treatment modalities target only HIV and not the HIV reservoirs. The impact of coexistence of HIV reservoirs in conjunction with M. tuberculosis is relatively an understudied area. Alveolar macrophages (AMs) harbor both M. tuberculosis and HIV. Clarke et al., established clinical evidence of HIV reservoirs in broncho-alveolar lavage (BAL) of ~43 of 78 patients [9]. Evidence of existence of HIV in lung reservoirs dates back to 1990 [10] where, HIV was known to infect AMs and fibroblasts.
Neuro-Ophthalmic Manifestations of HIV Infection
Published in Ocular Immunology and Inflammation, 2020
Lynn K. Gordon, Helen Danesh-Meyer
PML, an opportunistic infection caused by the John Cunningham (JC) virus, causes a demyelinating CNS disease that complicates conditions in which there is impaired cell-mediated immunity such as HIV.90 It is thought that JC virus latency is established in childhood after a common subclinical infection in childhood/early adulthood.91 In HIV immunosuppressed patients, there is reactivation of the infection. The virus reaches the CNS via hematogenous spread with a tropism for brain oligodendroglia.