Interference with complement regulatory molecules as a possible therapeutic strategy in HIV infection

Pintér, Claudia; Beltrami, Silvia; Stoiber, Heribert; Negri, Donatella; Titti, Fausto; Clivio, Alberto

doi:10.1517/13543784.9.2.199

Cited by 4 publications

(2 citation statements)

References 27 publications

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“…AIDS: The term "immunodeficiency", or maybe the more accurate term "immune-malfunction", expresses exactly what people observed in AIDS patients. HIV-1 virus escapes complement-mediated immune protection and remain highly infective, even though both the HIV-1 envelope antigens and anti-HIV specific antibodies in the serum of HIV-1 infected patients are able to active the complement cascade reactions as discussed above [32,52]. It is confirmed that HIV-1 virions isolated from infected individuals have accumulated C3 on their surface, a signal of the initiation of complement reactions, but HIV-1 virions are still very resistant to complement mediated killing, which is a different phenomenon of humoral immune responses induced from the most invaded pathogens [32].…”

Section: Critical Role Of Fh In Pathogenesis Of Several Dreadful Disementioning

confidence: 99%

Age to End Dreadful Diseases (HIV, Malaria, TB, Cancer and More): A Theory of Intact or Protected Complement (IPC) Immunity

Jin¹

2017

J Vaccines Vaccin

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After enormous efforts to fight for a successful HIV vaccine, the movement ended with frustration. While people are celebrating the victories of disease prophylaxis and healthy improvement, millions of them are still struggling on numerous unsettled dreadful illnesses, i.e., HIV, malaria, TB, cancer and autoimmune disorders. A theory of Intact or Protected Complement (IPC) immunity proposed in this review is to focus on hijacked complement system, the powerful leverage weapon restrained by many pathogens or cancer cells. The theory is to stimulate more investigations to discover the key block in continuous achievement in successful vaccine development and immune therapy.

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Section: Critical Role Of Fh In Pathogenesis Of Several Dreadful Disementioning

confidence: 99%

Age to End Dreadful Diseases (HIV, Malaria, TB, Cancer and More): A Theory of Intact or Protected Complement (IPC) Immunity

Jin¹

2017

J Vaccines Vaccin

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“…A short peptide derived from the binding site of fH to HIV was shown to compete with the binding of fH; reduced presence of fH-dependent control could thus induce complement-mediated killing of HIV or HIV-infected cells [reviewed in ref. 100]. Furthermore, the broadly neutralizing monoclonal antibody 2F5 recognises the fH-binding epitope of gp41 and thus undermines the resistance of HIV virions to complement attack.…”

Section: Aspect 4: Complement and Therapymentioning

confidence: 99%

Complement in Different Stages of HIV Infection and Pathogenesis

Speth¹,

Stoiber²,

Dierich³

2003

Int Arch Allergy Immunol

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The complement system is one of the most important weapons of innate immunity and is involved in all infectious processes. It is not only a mechanism for direct protection against an invading pathogen but it also interacts with the adaptive immunity to optimize the pathogen-specific humoral and cellular defence cascade in the body. One of the greatest challenges for the complement system is infection by HIV with its chronic course and sequential destruction of immune cells and immune organs. Due to its dual role as direct effector and as fine tuner of adaptive immunity, we focussed on complement in this review and analysed in detail the contribution of complement to the antiviral defence and to HIV pathogenesis on the one hand and the complement evasion strategies of the virus on the other hand. In the present review, this interplay between complement and the virus is illuminated for the three different stages of HIV pathogenesis and for events during therapy: (1) the acute infection process with the early events in mucosa and serum; (2) the asymptomatic stage with the complex interplay between complement-induced lysis and viral evasion strategies; (3) the symptomatic infection and AIDS stage with progressive destruction of the lymph nodes, opportunistic infections and development of neuropathogenesis, and (4) finally, during highly active antiretroviral therapy and in vaccination approaches.

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Antiviral Agents

Hosmane

2003

Kirk-Othmer Encyclopedia of Chemical Technology

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Since the discovery of the first virus >100 years ago, thousands of different viruses have been identified and characterized, and a number of plant, animal, and human ailments have been traced to viral origin. The rapid advances made in tools and techniques of molecular biology in the last 40 years, coupled with cooperative efforts in genetics and biochemical fronts, have afforded intricate details of the structure, function, replication, and genomic makeup of a host of viruses. As there are too many viruses to give even short accounts, this article focuses on only those that have some relevance to human diseases. But, since the list of all human viruses would still be too long to give detailed descriptions for each, the focus is further narrowed down to four major viruses that are currently perceived to threaten global health. These four viruses include HIV (human immunodeficiency virus, which causes AIDS), HBV and HCV (hepatitis B and C viruses that cause liver damage), and the more recent WNV (West Nile virus that causes brain inflammation). Nevertheless, an attempt has been made to classify all the known major viruses based on their shape, size, symmetry, hosts, and chemical composition that includes nucleic acid, protein, and presence or absence of lipid envelope. As they are a form of life that cannot replicate outside a host cell, viruses have evolved to develop complex and diverse interactions with higher organisms. Therefore, it was long believed that the development of antiviral agents that would specifically disrupt the viral replication process without affecting the normal metabolic events of the host would be difficult. Thanks to excellent advances in virology, several targets that are unique to the viruses have now been identified and successfully explored. This article briefly describes the general processes of viral infection to point out potential targets for selective antiviral agents. These targets are then classified into two major virus‐specific processes, including ( a ) early events of viral adsorption, penetration and uncoating, and ( b ) later synthetic events that concern intracellular replication of the virus. While there are only limited choices of candidates dealing with the early events, a much larger pool of candidates exists for targeting the later events in a virus life cycle, and they are known to be virus‐specific. The viruses synthesize and utilize specific enzymes and proteins, and more importantly, the replication of viral genomes is also virus‐specific. Nucleoside analogues which target these later events of viral life cycles have played major roles as antiviral agents against almost all the major viruses, and therefore, a special emphasis has been placed on this class of compounds in this review article. Prophylactic measures such as vaccine immunization have also been discussed under each of the four major viruses mentioned.

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Interference with complement regulatory molecules as a possible therapeutic strategy in HIV infection

Cited by 4 publications

References 27 publications

Age to End Dreadful Diseases (HIV, Malaria, TB, Cancer and More): A Theory of Intact or Protected Complement (IPC) Immunity

Age to End Dreadful Diseases (HIV, Malaria, TB, Cancer and More): A Theory of Intact or Protected Complement (IPC) Immunity

Complement in Different Stages of HIV Infection and Pathogenesis

Antiviral Agents

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