HIV-1 infected monozygotic twins

A tale of two outcomes

Loubna Rothenburg, Hiromi Imamichi, Steven Hirschfeld, Julia A. Metcalf, Susan Orsega, Marcos Pérez-Losada, David Posada, H. Clifford Lane, Keith A. Crandall

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Background. Replicate experiments are often difficult to find in evolutionary biology, as this field is inherently an historical science. However, viruses, bacteria and phages provide opportunities to study evolution in both natural and experimental contexts, due to their accelerated rates of evolution and short generation times. Here we investigate HIV-1 evolution by using a natural model represented by monozygotic twins infected synchronically at birth with an HIV-1 population from a shared blood transfusion source. We explore the evolutionary processes and population dynamics that shape viral diversity of HIV in these monozygotic twins. Results. Despite the identical host genetic backdrop of monozygotic twins and the identical source and timing of the HIV-1 inoculation, the resulting HIV populations differed in genetic diversity, growth rate, recombination rate, and selection pressure between the two infected twins. Conclusions. Our study shows that the outcome of evolution is strikingly different between these two "replicates" of viral evolution. Given the identical starting points at infection, our results support the impact of random epigenetic selection in early infection dynamics. Our data also emphasize the need for a better understanding of the impact of host-virus interactions in viral evolution.

Original languageEnglish (US)
Article number62
JournalBMC Evolutionary Biology
Volume11
Issue number1
DOIs
StatePublished - Mar 14 2011
Externally publishedYes

Fingerprint

human immunodeficiency virus
Human immunodeficiency virus 1
virus
viruses
blood transfusion
early selection
generation time
evolutionary biology
epigenetics
infection
bacteriophages
recombination
inoculation
population genetics
population dynamics
blood
Biological Sciences
genetic variation
bacterium
bacteria

ASJC Scopus subject areas

  • Ecology, Evolution, Behavior and Systematics

Cite this

Rothenburg, L., Imamichi, H., Hirschfeld, S., Metcalf, J. A., Orsega, S., Pérez-Losada, M., ... Crandall, K. A. (2011). HIV-1 infected monozygotic twins: A tale of two outcomes. BMC Evolutionary Biology, 11(1), [62]. https://doi.org/10.1186/1471-2148-11-62

HIV-1 infected monozygotic twins : A tale of two outcomes. / Rothenburg, Loubna; Imamichi, Hiromi; Hirschfeld, Steven; Metcalf, Julia A.; Orsega, Susan; Pérez-Losada, Marcos; Posada, David; Lane, H. Clifford; Crandall, Keith A.

In: BMC Evolutionary Biology, Vol. 11, No. 1, 62, 14.03.2011.

Research output: Contribution to journalArticle

Rothenburg, L, Imamichi, H, Hirschfeld, S, Metcalf, JA, Orsega, S, Pérez-Losada, M, Posada, D, Lane, HC & Crandall, KA 2011, 'HIV-1 infected monozygotic twins: A tale of two outcomes', BMC Evolutionary Biology, vol. 11, no. 1, 62. https://doi.org/10.1186/1471-2148-11-62
Rothenburg L, Imamichi H, Hirschfeld S, Metcalf JA, Orsega S, Pérez-Losada M et al. HIV-1 infected monozygotic twins: A tale of two outcomes. BMC Evolutionary Biology. 2011 Mar 14;11(1). 62. https://doi.org/10.1186/1471-2148-11-62
Rothenburg, Loubna ; Imamichi, Hiromi ; Hirschfeld, Steven ; Metcalf, Julia A. ; Orsega, Susan ; Pérez-Losada, Marcos ; Posada, David ; Lane, H. Clifford ; Crandall, Keith A. / HIV-1 infected monozygotic twins : A tale of two outcomes. In: BMC Evolutionary Biology. 2011 ; Vol. 11, No. 1.
@article{4bc4e0dbb71c4a54abf3875068a29907,
title = "HIV-1 infected monozygotic twins: A tale of two outcomes",
abstract = "Background. Replicate experiments are often difficult to find in evolutionary biology, as this field is inherently an historical science. However, viruses, bacteria and phages provide opportunities to study evolution in both natural and experimental contexts, due to their accelerated rates of evolution and short generation times. Here we investigate HIV-1 evolution by using a natural model represented by monozygotic twins infected synchronically at birth with an HIV-1 population from a shared blood transfusion source. We explore the evolutionary processes and population dynamics that shape viral diversity of HIV in these monozygotic twins. Results. Despite the identical host genetic backdrop of monozygotic twins and the identical source and timing of the HIV-1 inoculation, the resulting HIV populations differed in genetic diversity, growth rate, recombination rate, and selection pressure between the two infected twins. Conclusions. Our study shows that the outcome of evolution is strikingly different between these two {"}replicates{"} of viral evolution. Given the identical starting points at infection, our results support the impact of random epigenetic selection in early infection dynamics. Our data also emphasize the need for a better understanding of the impact of host-virus interactions in viral evolution.",
author = "Loubna Rothenburg and Hiromi Imamichi and Steven Hirschfeld and Metcalf, {Julia A.} and Susan Orsega and Marcos P{\'e}rez-Losada and David Posada and Lane, {H. Clifford} and Crandall, {Keith A.}",
year = "2011",
month = "3",
day = "14",
doi = "10.1186/1471-2148-11-62",
language = "English (US)",
volume = "11",
journal = "BMC Evolutionary Biology",
issn = "1471-2148",
publisher = "BioMed Central",
number = "1",

}

TY - JOUR

T1 - HIV-1 infected monozygotic twins

T2 - A tale of two outcomes

AU - Rothenburg, Loubna

AU - Imamichi, Hiromi

AU - Hirschfeld, Steven

AU - Metcalf, Julia A.

AU - Orsega, Susan

AU - Pérez-Losada, Marcos

AU - Posada, David

AU - Lane, H. Clifford

AU - Crandall, Keith A.

PY - 2011/3/14

Y1 - 2011/3/14

N2 - Background. Replicate experiments are often difficult to find in evolutionary biology, as this field is inherently an historical science. However, viruses, bacteria and phages provide opportunities to study evolution in both natural and experimental contexts, due to their accelerated rates of evolution and short generation times. Here we investigate HIV-1 evolution by using a natural model represented by monozygotic twins infected synchronically at birth with an HIV-1 population from a shared blood transfusion source. We explore the evolutionary processes and population dynamics that shape viral diversity of HIV in these monozygotic twins. Results. Despite the identical host genetic backdrop of monozygotic twins and the identical source and timing of the HIV-1 inoculation, the resulting HIV populations differed in genetic diversity, growth rate, recombination rate, and selection pressure between the two infected twins. Conclusions. Our study shows that the outcome of evolution is strikingly different between these two "replicates" of viral evolution. Given the identical starting points at infection, our results support the impact of random epigenetic selection in early infection dynamics. Our data also emphasize the need for a better understanding of the impact of host-virus interactions in viral evolution.

AB - Background. Replicate experiments are often difficult to find in evolutionary biology, as this field is inherently an historical science. However, viruses, bacteria and phages provide opportunities to study evolution in both natural and experimental contexts, due to their accelerated rates of evolution and short generation times. Here we investigate HIV-1 evolution by using a natural model represented by monozygotic twins infected synchronically at birth with an HIV-1 population from a shared blood transfusion source. We explore the evolutionary processes and population dynamics that shape viral diversity of HIV in these monozygotic twins. Results. Despite the identical host genetic backdrop of monozygotic twins and the identical source and timing of the HIV-1 inoculation, the resulting HIV populations differed in genetic diversity, growth rate, recombination rate, and selection pressure between the two infected twins. Conclusions. Our study shows that the outcome of evolution is strikingly different between these two "replicates" of viral evolution. Given the identical starting points at infection, our results support the impact of random epigenetic selection in early infection dynamics. Our data also emphasize the need for a better understanding of the impact of host-virus interactions in viral evolution.

UR - http://www.scopus.com/inward/record.url?scp=79952353614&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79952353614&partnerID=8YFLogxK

U2 - 10.1186/1471-2148-11-62

DO - 10.1186/1471-2148-11-62

M3 - Article

VL - 11

JO - BMC Evolutionary Biology

JF - BMC Evolutionary Biology

SN - 1471-2148

IS - 1

M1 - 62

ER -