Identification of a human population infected with simian foamy viruses

Heneine, Walid; Switzer, William M.; Sandstrom, Paul; Brown, Jennifer L.; Shanmugam, Vedapuri; Schable, Charles A.; Khan, Arifa S.; Lerche, Nicholas W.; Schweizer, Matthias; Neumann‐Haefelin, Dieter; Chapman, Louisa E.; Folks, Thomas M.

doi:10.1038/nm0498-403

Cited by 210 publications

(196 citation statements)

References 29 publications

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“…Based on extensive nucleotide and amino-acid homology (Herchenröder et al, 1994), the foamy virus originally isolated from a human (ie, 'human foamy virus') may actually be identical to a chimpanzee simian foamy virus isolate (SFVcpz). Indeed, the African patient from whom HFV was first isolated could have acquired the virus from a primate (Meiering and Linial, 2001), since such transmission of SFV can occur through close animal contact (Schweitzer et al, 1997;Heneine et al, 1998;Sandstrom et al, 2000;Brooks et al, 2002). Alternatively, the initial report may have represented a laboratory contamination (Meiering and Linial, 2001).…”

Section: B Amentioning

confidence: 99%

“…Although evidence for infection with HFV (or a closely related primate virus) has been reported in patients with a range of autoimmune or idiopathic diseases, including Graves' disease, thyroiditis de Quervain, and multiple sclerosis, later studies cast doubts on those findings (Meiering and Linial, 2001). Documented human infection with SFV has not been linked to disease (Schweitzer et al, 1997;Heneine et al, 1998;Brooks et al, 2002).…”

Section: B Amentioning

confidence: 99%

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Absence of human T-cell lymphotropic virus type I and human foamy virus in thymoma

Loehrer

Hisada

et al. 2004

Br J Cancer

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The cause of thymoma, a rare malignancy of thymic epithelial cells, is unknown. Recent studies have reported the detection of DNA from human T-cell lymphotropic virus type I (HTLV-I) and human foamy virus (HFV) in small numbers of thymoma tumours, suggesting an aetiologic role for these retroviruses. In the present study, we evaluated 21 US thymoma patients and 20 patients with other cancers for evidence of infection with these viruses. We used the polymerase chain reaction to attempt to amplify viral DNA from tumour tissues, using primers from the pol and tax (HTLV-I) and gag and bel1 (HFV) regions. In these experiments, we did not detect HTLV-I or HFV DNA sequences in any thymoma or control tissues, despite adequate sensitivity of our assays (one HTLV-I copy per 25

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Section: B Amentioning

confidence: 99%

Section: B Amentioning

confidence: 99%

Absence of human T-cell lymphotropic virus type I and human foamy virus in thymoma

Loehrer

Hisada

et al. 2004

Br J Cancer

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“…Table 4, although certainly incomplete, summarizes many reports of these cross-infections [58,[65][66][67][68][69][70][71][72][73][74][75][76][77][78][79][80][81][82][83]. Of particular interest is the evidence that the simian T cell lymphotropic virus 1 of chimps was transmitted to humans, where it evolved into human T cell lymphotropic virus type 1 (A.-M. Vandamme, personal communication) [68,70].…”

Section: Cross-infection Between Primate Speciesmentioning

confidence: 99%

CHAT Oral Polio Vaccine Was Not the Source of Human Immunodeficiency Virus Type 1 Group M for Humans

Gellin

Modlin

Plotkin

2001

Clinical Infectious Diseases

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A book published in 1999 hypothesized that the scientists who worked with the CHAT type 1 attenuated poliomyelitis strain, tested in the former Belgian Congo in the late 1950s, had covertly prepared the vaccine in chimpanzee kidney cells contaminated with a simian immunodeficiency virus, which evolved into human immunodeficiency virus type 1 group M. This article summarizes the results of the investigation conducted by the author to determine the legitimacy of the accusation. Testimony by eyewitnesses, historical documents of the time, epidemiological analysis, and analysis of ancillary phylogenetic, virological, and polymerase chain reaction data all indicate that this hypothesis is false.Poliomyelitis is rapidly disappearing from the world, thanks in large part to the widespread use of the oral polio vaccine (OPV) strains developed by Albert Sabin. The precursors of the Sabin strains were those developed by Hilary Koprowski, first at the Lederle Laboratories and then at the Wistar Institute in Philadelphia. The results of the first administration of OPV to humans were published by Koprowski et al. in 1952 [1] and concerned the TN strain, later identified as type 2 poliovirus. A type 1 strain, called SM, was reported in 1954 [2], and its descendant, a virus called "CHAT" was reported in 1957 [3]. The latter strain concerns us here, for in 1999, a British journalist published a book called The River: A Journal to the Source of HIV and AIDS [4], which proposed the hypothesis that CHAT had been produced in cells from chimpanzees that were contaminated with the simian precursor of HIV type 1 (HIV-1) group M, the major agent of the AIDS epidemic. This article examines that hypothesis in detail.For a proper understanding of the events recalled in this article, the state of polio vaccine development in the late 1950s is germane. In the late 1950s, obtaining cultures of kidney cells from rhesus monkeys was routine, and commercial laboratories were selling trypsinized kidneys or monolayer cultures in glass bottles. The plaque technique of Dulbecco and Vogt had also come into general use, permitting for the first time cloning (in the old sense) of genetically distinct virus populations. (Therefore, whereas both the early TN type 2 and SM type 1 attenuated strains of Koprowski had been attenuated in rodents, the SM strain was then further attenuated by alternate passages in chick embryo and cultures of monkey kidney cells.) However, the SM strain appeared to be too neurovirulent [5,6], and a substrain called SM-N90 was passed 4 times serially in humans by oral administration of filtered fecal virus, isolated after replication in the intestine. After the fourth human passage, the virus was plaqued 4 times ("plaque purification") in cultures of monkey kidney cells, and the resultant strain was renamed CHAT, after the name of the baby in whom the last human passage had been made.The plaque passage history was shown in detail in Koprowski's article ( figure 1) [3] . The sequence of plaque passage was plaque 9 to plaque 13 to...

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“…In addition, in contrast to all other retroviruses used for gene therapy, no known diseases have been associated with naturally occurring FV infections in cats, horses, chimpanzees, orangutans, and cows [12]. While there are several cases of health care providers in zoos who have accidentally contracted simian FV, none of these individuals have developed any symptoms or transmitted the virus to other humans despite the chronic persistent infection [13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

In vivo selection of hematopoietic stem cells transduced at a low multiplicity-of-infection with a foamy viral MGMTP140K vector

Cai¹,

Ernstberger²,

Wang³

et al. 2008

Experimental Hematology

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Objective-Using a clinically relevant transduction strategy, we investigated to what extent hematopoietic stem cells in lineage-negative bone marrow (Lin neg BM) could be genetically modified with a FV vector that expresses the DNA repair protein, O 6 -methylguanine DNA methyltransferase (MGMT P140K ) and selected in vivo with submyeloablative versus myeloablative alkylator therapy.Methods-Lin neg BM was transduced at a low multiplicity-of-infection (MOI), with the FV vector, MD9-P140K, that co-expresses MGMT P140K and the enhanced green fluorescent protein, transplanted into C57BL/6 mice, and mice treated with submyeloablative or myeloablative alkylator therapy. The BM was analyzed for the presence of in vivo selected, MD9-P140K-transduced cells at 6 months post-transplantation and subsequently transplanted into secondary recipient animals.Results-Following submyeloablative therapy, 55% of the mice expressed MGMT P140K in the BM. Proviral integration was observed in ∼50% of committed BM-derived progenitors and analysis of proviral insertion sites indicated up to 2 integrations per transduced progenitor colony. Transduced BM cells selected with submyeloablative therapy reconstituted secondary recipient mice for up to 6 months post-transplantation. In contrast, following delivery of myeloablative therapy to primary recipient mice, only 25% survived. Hematopoietic stem cells were transduced since BM cells from the surviving animals reconstituted secondary recipients with MGMT P140K positive cells for 5-6 months. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. of transduced-stem cells must be present to produce sufficient numbers of genetically modified progeny to protect against the acute toxicity associated with myeloablative therapy. Conclusions-In NIH Public Access

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Identification of a human population infected with simian foamy viruses

Cited by 210 publications

References 29 publications

Absence of human T-cell lymphotropic virus type I and human foamy virus in thymoma

Absence of human T-cell lymphotropic virus type I and human foamy virus in thymoma

CHAT Oral Polio Vaccine Was Not the Source of Human Immunodeficiency Virus Type 1 Group M for Humans

In vivo selection of hematopoietic stem cells transduced at a low multiplicity-of-infection with a foamy viral MGMTP140K vector

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