Recombinant viruses and early global HIV-1 epidemic.
Ontology highlight
ABSTRACT:
SUBMITTER: Kalish ML
PROVIDER: S-EPMC3323344 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The global paediatric HIV epidemic is shifting into a new phase as children on antiretroviral therapy (ART) move into adolescence and adulthood, and face new challenges of living with HIV. UNAIDS reports that 3.4 million children aged below 15 years and 2 million adolescents aged between 10 and 19 years have HIV. Although the vast majority of children were perinatally infected, older children are combined with behaviourally infected adolescents and youth in global reporting, making it difficult to keep track of their outcomes. Perinatally HIV-infected adolescents (PHIVA) are a highly unique patient sub-population, having been infected before development of their immune systems, been subject to suboptimal ART options and formulations, and now face transition from complete dependence on adult caregivers to becoming their own caregivers. As we are unable to track long-term complications and survival of PHIVA through national and global reporting systems, local and regional cohorts are the main sources for surveillance and research among PHIVA. This global review will utilize those data to highlight the epidemiology of PHIVA infection, treatment challenges and chronic disease risks. Unless mechanisms are created to count and separate out PHIVA outcomes, we will have few opportunities to characterize the negative consequences of life-long HIV infection in order to find ways to prevent them.
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Project description:Thirty years after the discovery of HIV-1, the early transmission, dissemination, and establishment of the virus in human populations remain unclear. Using statistical approaches applied to HIV-1 sequence data from central Africa, we show that from the 1920s Kinshasa (in what is now the Democratic Republic of Congo) was the focus of early transmission and the source of pre-1960 pandemic viruses elsewhere. Location and dating estimates were validated using the earliest HIV-1 archival sample, also from Kinshasa. The epidemic histories of HIV-1 group M and nonpandemic group O were similar until ~1960, after which group M underwent an epidemiological transition and outpaced regional population growth. Our results reconstruct the early dynamics of HIV-1 and emphasize the role of social changes and transport networks in the establishment of this virus in human populations.
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Project description:We systematically evaluated multiple and recombinant infections in an HIV-infected population selected for vaccine trials. Seventy-nine HIV-1 infected persons in a clinical cohort study in Rio de Janeiro, Brazil, were evaluated for 1 year. A combination of molecular screening assays and DNA sequencing showed 3 dual infections (3.8%), 6 recombinant infections (7.6%), and 70 (88.6%) infections involving single viral subtypes. In the three dual infections, we identified HIV-1 subtypes F and B, F and D, and B and D; in contrast, the single and recombinant infections involved only HIV-1 subtypes B and F. The recombinants had five distinct B/F mosaic patterns: Bgag-p17/Bgag-p24/Fpol/Benv, Fgag-p17/Bgag-p24/Fpol/Fenv, Bgag-p17/B-Fgag-p24/Fpol/Fenv, Bgag-p17/B-Fgag-p24/Fpol/Benv, and Fgag-p17/B-Fgag-p24/Fpol/Fenv. No association was found between dual or recombinant infections and demographic or clinical variables. These findings indicate that dual and recombinant infections are emerging as an integral part of the HIV/AIDS epidemic in Brazil and emphasize the heterogenous character of epidemics emerging in countries where multiple viral subtypes coexist.
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Project description:ObjectiveTo better understand the global response to HIV/AIDS, this study tracked development assistance for HIV/AIDS at a granular, program level.MethodsWe extracted data from the Institute for Health Metrics and Evaluation's Financing Global Health 2015 report that captured development assistance for HIV/AIDS from 1990 to 2015 for all major bilateral and multilateral aid agencies. To build on these data, we extracted additional budget data, and disaggregated development assistance for HIV/AIDS into nine program areas, including prevention, treatment, and health system support.ResultsSince 2000, $109.8 billion of development assistance has been provided for HIV/AIDS. Between 2000 and 2010, development assistance for HIV/AIDS increased at an annualized rate of 22.8%. Since 2010, the annualized rate of growth has dropped to 1.3%. Had development assistance for HIV/AIDS continued to climb after 2010 as it had in the previous decade, $44.8 billion more in development assistance would have been available for HIV/AIDS. Since 1990, treatment and prevention were the most funded HIV/AIDS program areas receiving $24.6 billion and $22.7 billion, respectively. Since 2010, these two program areas and HIV/AIDS health system strengthening have continued to grow, marginally, with majority support from the US government and the Global Fund. An average of $252.9 of HIV/AIDS development assistance per HIV/AIDS prevalent case was disbursed between 2011 and 2013.ConclusionThe scale-up of development assistance for HIV/AIDS from 2000 to 2010 was unprecedented. During this period, international donors prioritized HIV/AIDS treatment, prevention, and health system support. Since 2010, funding for HIV/AIDS has plateaued.
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Project description:This a model from the article:
Fighting a virus with a virus: a dynamic model for HIV-1 therapy.
Revilla T, Garcia-Ramos G. Math Biosci
2003 Oct;185(2):191-203 12941536
,
Abstract:
A mathematical model examined a potential therapy for controlling viral
infections using genetically modified viruses. The control of the infection is
an indirect effect of the selective elimination by an engineered virus of
infected cells that are the source of the pathogens. Therefore, this engineered
virus could greatly compensate for a dysfunctional immune system compromised by
AIDS. In vitro studies using engineered viruses have been shown to decrease the
HIV-1 load about 1000-fold. However, the efficacy of this potential treatment
for reducing the viral load in AIDS patients is unknown. The present model
studied the interactions among the HIV-1 virus, its main host cell (activated
CD4+ T cells), and a therapeutic engineered virus in an in vivo context; and it
examined the conditions for controlling the pathogen. This model predicted a
significant drop in the HIV-1 load, but the treatment does not eradicate HIV. A
basic estimation using a currently engineered virus indicated an HIV-1 load
reduction of 92% and a recovery of host cells to 17% of their normal level.
Greater success (98% HIV reduction, 44% host cells recovery) is expected as more
competent engineered viruses are designed. These results suggest that therapy
using viruses could be an alternative to extend the survival of AIDS patients.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Revilla T, Garcia-Ramos G. (2003) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2024-09-02 | BIOMD0000000707 | BioModels
Project description:HIV-1 subtype C is the most prevalent subtype in South Africa. Although subtype B was previously detected in South Africa, there is limited sequence information available. We characterized near full-length HIV-1 subtype B sequences from samples collected at the start of the South African HIV-1 epidemic, in the 1980s. Five samples were analysed by PCR amplification, Sanger DNA sequencing and phylogenetic analyses. The viral genomes were amplified in two overlapping fragments of 5.5 kb and 3.7 kb. The sequences were subtyped using REGA version 3.0, RIP version 3.0 and jpHMM. Maximum Likelihood phylogenetic trees were inferred with MEGA version 6. Four HIV-1 patient sequences were subtyped as pure HIV-1 subtype B. One sequence was characterized as a novel HIV-1 subtype B and D recombinant. The sequences clustered phylogenetically with other HIV-1 subtype B sequences from South Africa, Europe and the USA. We report the presence of an HIV-1 subtype B and D recombinant strain detected in the beginning of the epidemic. This indicates that viral recombination events were already happening in 1985, but could have been missed as sequence analyses were often limited to small genomic regions of HIV-1.
| S-EPMC6470202 | biostudies-literature
Project description:Recombinant viruses are novel therapeutic agents that can be utilized for treatment of various diseases, including cancers. Recombinant viruses can be engineered to express foreign transgenes and have a broad tropism allowing gene expression in a wide range of host cells. They can be selected or designed for specific therapeutic goals; for example, recombinant viruses could be used to stimulate host immune response against tumor-specific antigens and therefore overcome the ability of the tumor to evade the host's immune surveillance. Alternatively, recombinant viruses could express immunomodulatory genes which stimulate an anti-cancer immune response. Oncolytic viruses can replicate specifically in tumor cells and induce toxic effects leading to cell lysis and apoptosis. However, each of these approaches face certain difficulties that must be resolved to achieve maximum therapeutic efficacy. In this review we discuss actively developing approaches for cancer therapy based on recombinant viruses, problems that need to be overcome, and possible prospects for further development of recombinant virus based therapy.
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