Clearance of HIV Infection in a Perinatally Infected Infant

Bryson, Yvonne J.; Pang, Shen; Wei, Lian S.; Dickover, Ruth; Diagne, Amadou; Chen, Irvin S. Y.

doi:10.1097/00006254-199510000-00010

Cited by 13 publications

(15 citation statements)

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“…In contrast, the active production of HIV-1 IgA and IgG antibodies was not observed in Patients 2 and 3, even though high titers of infectious virus were isolated from their plasma and PBMCs for several weeks before therapy. This finding is compatible with one of documented seroreversion in an infant recently reported to have had clearance of maternally acquired HIV-1 infection 19 and with the transient, low-level antibody production in neonatal macaques with limited replication of simian immunodeficiency virus in early infection. 20 The presence of high titers of maternal HIV-1 antibody when viral replication began may have dampened primary humoral immune responses.…”

Section: Discussionsupporting

confidence: 89%

Combination Treatment with Zidovudine, Didanosine, and Nevirapine in Infants with Human Immunodeficiency Virus Type 1 Infection

et al. 1997

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Section: Discussionsupporting

confidence: 89%

Combination Treatment with Zidovudine, Didanosine, and Nevirapine in Infants with Human Immunodeficiency Virus Type 1 Infection

et al. 1997

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“…To our knowledge, the lowest reported plasma viral load during seroconversion is more than 17 times higher than the highest viral load detected in our three patients (7). Although transient HIV infection has been reported in infants, it is unlikely in two of our patients because they had not recently been exposed to HIV (8,9). Other potential explanations of false-positive HIV-1 plasma viral load include laboratory error, crosscontamination, and mix-up of specimens.…”

Section: Discussioncontrasting

confidence: 54%

Misdiagnosis of HIV Infection by HIV-1 Plasma Viral Load Testing: A Case Series

Rich

Merriman²,

Mylonakis³

et al. 1999

Ann Intern Med

106

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“…These individuals are regularly exposed to various HIV-1 strains due to unprotected sex (reviewed by Kaul et al 2002). Numerous additional reports indicate that certain individuals or groups are immune to HIV-1 altogether (Baur et al 1989, Bryson et al 1995, Deacon et al 1995, Roques et al 1995, Paxton et al 1996, Kaul et al 2000, Kulkarni et al 2003, while others remain AIDS free for extensive periods of time . In order to develop sufficient human protection against HIV-1 variants, a number of homologous sequences will be required in the endogenous repertoire (Hiroshika et al 2000, Donze & Picard 2002, Hohjoh 2002, Jeong et al 2002, Leirdal & Sioud 2002, Miyagishi & Taira 2002, Paddison et al 2002, Paul et al 2002, Sui et al 2002, Yu et al 2002.…”

Section: Role Of Sirnas In Development Of Hiv-1 Vaccinementioning

confidence: 99%

RNA interference: The molecular immune system

Bagasra

Prilliman²

2004

Histochem J

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SummaryIntroduction of double-stranded RNA (dsRNA) into cells expressing a homologous gene triggers RNA interference (RNAi), or RNA-based gene silencing (RBGS). The dsRNA degrades corresponding host mRNA into small interfering RNAs (siRNAs) by a protein complex containing Dicer. siRNAs in turn are incorporated into the RNA-induced silencing complex (RISC) that includes helicase, RecA, and exo-and endo-nucleases as well as other proteins. Following its assembly, the RISC guides the RNA degradation machinery to the target RNAs and cleaves the cognate target RNA in a sequence-specific, siRNA-dependent manner. RNAi has now been documented in a wide variety of organisms, including plants, fungi, flies, worms, and more recently, higher mammals. In eukaryotes, dsRNA directed against a range of viruses (i.e., HIV-1, RSV, HPV, poliovirus and others) and endogenous genes can induce sequence-specific inhibition of gene expression. In invertebrates, RNAi can be efficiently triggered by either long dsRNAs or 21-to 23-nt-long siRNAs. However, in jawed vertebrates, dsRNA longer than 30 bp can induce interferon and thus trigger undesirable side effects instead of initiating RNAi. siRNAs have been shown to act as potent inducers of RNAi in cultured mammalian cells. Many investigators have suggested that siRNAs may have evolved as a normal defense against endogenous and exogenous transposons and retroelements. Through a combination of genetic and biochemical approaches, some of the mechanisms underlying RNAi have been described. Recent data in C. elegans shows that two homologs of siRNAs, microRNAs (miRNAs) and tiny noncoding RNAs (tncRNAs) are endogenously expressed. However, many aspects of RNAi-induced gene silencing, including its origins and the selective pressures which maintain it, remain undefined. Its evolutionary history may pass through the more primitive immune functions of prokaryotes involving restriction enzymes that degrade plasmid DNA molecules that enter bacterial cells. RNAi has evolved further among eukaryotes, in which its wide distribution suggests early origins. RNAi seems to be involved in a variety of regulatory and immune functions that may differ among various kingdoms and phyla. We present here proposed mechanisms by which RBGS protects the host against endogenous and exogenous transposons and retroelements. The potential for therapeutic application of RBGS technology in treating viral infections such as HIV is also discussed.

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Clearance of HIV Infection in a Perinatally Infected Infant

Cited by 13 publications

References 0 publications

Combination Treatment with Zidovudine, Didanosine, and Nevirapine in Infants with Human Immunodeficiency Virus Type 1 Infection

Combination Treatment with Zidovudine, Didanosine, and Nevirapine in Infants with Human Immunodeficiency Virus Type 1 Infection

Misdiagnosis of HIV Infection by HIV-1 Plasma Viral Load Testing: A Case Series

RNA interference: The molecular immune system

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