scholarly journals Pengklonaan Plasmid Rekombinan gp125-gp36 Human Immunodeficiency Virus tipe 2 (HIV-2) untuk Pengembangan Sistem Diagnostik HIV-2

2019 ◽  
Vol 8 (1) ◽  
pp. 59-66
Author(s):  
Fathurrohim Fathurrohim ◽  
Silvia Tri Widyaningtyas ◽  
Budiman Bela
Keyword(s):  
Immune Deficiency ◽  
Human Immunodeficiency Virus ◽  
Immune Deficiency Syndrome ◽  
Acquired Immune Deficiency Syndrome ◽  
Deficiency Syndrome ◽  
Rapid Diagnostic Tests ◽  
Immunodeficiency Virus ◽  
Acquired Immune Deficiency ◽  
Anti Hiv ◽  
Hiv 1

AbstractFrom 36.9 million people infected by the Human Immunodeficiency Virus (HIV) at the end of 2018 in the whole world, 1-2 million are infected by HIV-2. Accurately diagnostic is required to ensure whether an individual has been infected HIV-1, HIV-2, or HIV-1 and HIV-2 co-infection. HIV-2 diagnostic error using rapid diagnostic tests (RDT) frequently occurs. Misdiagnostic of HIV-2 infection may cause treatment failure which leads to the development of Acquired Immune Deficiency Syndrome (AIDS). In this study, expression plasmid pQE80L-gp125-gp36 HIV-2 that can produce recombinant antigen gp125-gp36 HIV-2 was successfully constructed and verified properly. The antigen is based on multiepitope, immunodominant and sustainable properties obtained by bioinformatics study. Plasmid pQE80L-gp125-gp36 HIV-2 may be used to produce recombinant antigens that benefit to detect anti-HIV-2 antibodies in an individual. AbstrakDari 36,9 juta individu yang terinfeksi oleh Human Immunodeficiency Virus (HIV) pada akhir tahun 2018 di seluruh dunia, terdapat sekitar 1 – 2 juta individu yang terinfeksi dengan HIV-2. Diagnostik yang akurat diperlukan untuk menentukan apakah suatu individu telah terinfeksi HIV-1, HIV-2 atau koinfeksi HIV-1 dan HIV-2. Kesalahan diagnostik HIV-2 menggunakan rapid diagnostic tests (RDT) sering sekali terjadi. Misdiagnosis infeksi HIV-2 dapat menyebabkan kegagalan pengobatan yang berujung pada perkembangan Acquired Immune Deficiency Syndrome (AIDS). Pada penelitian ini plasmid pQE80L-gp125-gp36 HIV-2 pengekspresi antigen rekombinan gp125-gp36 HIV-2 telah berhasil dikonstruksi dan terverifikasi dengan baik. Antigen tersebut berbasis multiepitop, immunodominan dan bersifat lestari yang didapatkan dari studi bioinformatik. Plasmid pQE80L-gp125-gp36 HIV-2 dapat digunakan untuk memproduksi antigen rekombinan yang dapat dimanfaatkan untuk mendeteksi antibodi anti HIV-2 pada suatu individu.

scholarly journals The earliest cases of human immunodeficiency virus type 1 group M in Congo-Kinshasa, Rwanda and Burundi and the origin of acquired immune deficiency syndrome

2001 ◽  
Vol 356 (1410) ◽  
pp. 923-925 ◽  
Author(s):  
Daniel Vangroenweghe
Keyword(s):  
Immune Deficiency ◽  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Immune Deficiency Syndrome ◽  
Acquired Immune Deficiency Syndrome ◽  
Deficiency Syndrome ◽  
Immunodeficiency Virus ◽  
Acquired Immune Deficiency ◽  
Hiv 1

The early cases of acquired immune deficiency syndrome and human immunodeficiency virus type 1 (HIV–1) infection in the 1960s and 1970s in Congo–Kinshasa (Zaire), Rwanda and Burundi are reviewed. These countries appear to be the source of the HIV–1 group M epidemic, which then spread outwards to neighbouring Tanzania and Uganda in the east, and Congo–Brazzaville in the west. Further spread to Haiti and onwards to the USA can be explained by the hundreds of single men from Haiti who participated in the UNESCO educational programme in the Congo between 1960 and 1975.

scholarly journals Using human immunodeficiency virus type 1 sequences to infer historical features of the acquired immune deficiency syndrome epidemic and human immunodeficiency virus evolution

2001 ◽  
Vol 356 (1410) ◽  
pp. 855-866 ◽  
Author(s):  
Karina Yusim ◽  
Martine Peeters ◽  
Oliver G. Pybus ◽  
Tanmoy Bhattacharya ◽  
Eric Delaporte ◽  
...  
Keyword(s):  
Immune Deficiency ◽  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Immune Deficiency Syndrome ◽  
Acquired Immune Deficiency Syndrome ◽  
Deficiency Syndrome ◽  
Immunodeficiency Virus ◽  
Acquired Immune Deficiency ◽  
Hiv 1

In earlier work, human immunodeficiency virus type 1 (HIV–1) sequences were analysed to estimate the timing of the ancestral sequence of the main group of HIV–1, the virus that is responsible for the acquired immune deficiency syndrome pandemic, yielding a best estimate of 1931 (95% confidence interval of 1915–1941). That work will be briefly reviewed, outlining how phylogenetic tools were extended to incorporate improved evolutionary models, how the molecular clock model was adapted to incorporate variable periods of latency, and how the approach was validated by correctly estimating the timing of two historically documented dates. The advantages, limitations, and assumptions of the approach will be summarized, with particular consideration of the implications of branch length uncertainty and recombination. We have recently undertaken new phylogenetic analysis of an extremely diverse set of human immunodeficiency virus envelope sequences from the Democratic Republic of the Congo (the DRC, formerly Zaire). This analysis both corroborates and extends the conclusions of our original study. Coalescent methods were used to infer the demographic history of the HIV–1 epidemic in the DRC, and the results suggest an increase in the exponential growth rate of the infected population through time.

scholarly journals Epidemiology and the emergence of human immunodeficiency virus and acquired immune deficiency syndrome

2001 ◽  
Vol 356 (1410) ◽  
pp. 795-798 ◽  
Author(s):  
Kevin M. De Cock
Keyword(s):  
Immune Deficiency ◽  
Human Immunodeficiency Virus ◽  
Immune Deficiency Syndrome ◽  
Acquired Immune Deficiency Syndrome ◽  
Deficiency Syndrome ◽  
Hiv And Aids ◽  
Immunodeficiency Virus ◽  
Ecological Association ◽  
Acquired Immune Deficiency ◽  
Hiv 1

Although acquired immune deficiency syndrome (AIDS) was first described in the USA in 1981, there is evidence that individual cases occurred considerably earlier in Central Africa, and serological and virological data show human immunodeficiency virus (HIV) was present in the Democratic Republic of Congo (DRC) as far back as 1959. It is likely that HIV–1 infection in humans was established from cross–species transmission of simian immunodeficiency virus of chimpanzees, but the circumstances surrounding this zoonotic transfer are uncertain. This presentation will review how causality is established in epidemiology, and review the evidence (a putative ecological association) surrounding the hypothesis that early HIV–1 infections were associated with trials of oral polio vaccine (OPV) in the DRC. From an epidemiological standpoint, the OPV hypothesis is not supported by data and the ecological association proposed between OPV use and early HIV/AIDS cases is unconvincing. It is likely that Africa will continue to dominate global HIV and AIDS epidemiology in the near to medium–term future, and that the epidemic will evolve over many decades unless a preventive vaccine becomes widely available.

scholarly journals The origin of acquired immune deficiency syndrome: Darwinian or Lamarckian?

2001 ◽  
Vol 356 (1410) ◽  
pp. 877-887 ◽  
Author(s):  
Tom Burr ◽  
J. M. Hyman ◽  
Gerald Myers
Keyword(s):  
Immune Deficiency ◽  
Simulated Data ◽  
Immune Deficiency Syndrome ◽  
Acquired Immune Deficiency Syndrome ◽  
Deficiency Syndrome ◽  
Darwinian Evolution ◽  
Immunodeficiency Virus ◽  
Acquired Immune Deficiency ◽  
Hiv 1

The subtypes of human immunodeficiency virus type 1 (HIV–1) group M exhibit a remarkable similarity in their between–subtype distances, which we refer to as high synchrony. The shape of the phylogenetic tree of these subtypes is referred to as a sunburst to distinguish it from a simple star phylogeny. Neither a sunburst pattern nor a comparable degree of symmetry is seen in a natural process such as in feline immunodeficiency virus evolution. We therefore have undertaken forward–process simulation studies employing coalescent theory to investigate whether such highly synchronized subtypes could be readily produced by natural Darwinian evolution. The forward model includes both classical (macro) and molecular (micro) epidemiological components. HIV–1 group M subtype synchrony is quantified using the standard deviation of the between–subtype distances and the average of the within–subtype distances. Highly synchronized subtypes and a sunburst phylogeny are not observed in our simulated data, leading to the conclusion that a quasi–Lamarckian, punctuated event occurred. The natural transfer theory for the origin of human acquired immune deficiency syndrome (AIDS) cannot easily be reconciled with these findings and it is as if a recent non–Darwinian process took place coincident with the rise of AIDS in Africa.

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