PMID- 18003730
OWN - NLM
STAT- MEDLINE
DCOM- 20080124
LR  - 20211020
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Print)
IS  - 0022-538X (Linking)
VI  - 82
IP  - 2
DP  - 2008 Jan
TI  - New world clade B arenaviruses can use transferrin receptor 1 (TfR1)-dependent 
      and -independent entry pathways, and glycoproteins from human pathogenic strains 
      are associated with the use of TfR1.
PG  - 938-48
AB  - Arenaviruses are rodent-borne viruses, with five members of the family capable of 
      causing severe hemorrhagic fevers if transmitted to humans. To date, two distinct 
      cellular receptors have been identified that are used by different pathogenic 
      viruses, alpha-dystroglycan by Lassa fever virus and transferrin receptor 1 
      (TfR1) by certain New World clade B viruses. Our previous studies have suggested 
      that other, as-yet-unknown receptors are involved in arenavirus entry. In the 
      present study, we examined the use of TfR1 by the glycoproteins (GPs) from a 
      panel of New World clade B arenaviruses comprising three pathogenic and two 
      nonpathogenic strains. Interestingly, we found that TfR1 was only used by the GPs 
      from the pathogenic viruses, with entry of the nonpathogenic strains being TfR1 
      independent. The pathogenic GPs could also direct entry into cells by 
      TfR1-independent pathways, albeit less efficiently. A comparison of the abilities 
      of TfR1 orthologs from different species to support arenavirus entry found that 
      the human and feline receptors were able to enhance entry of the pathogenic 
      strains, but that neither the murine or canine forms were functional. Since the 
      ability to use TfR1 is a characteristic feature of the human pathogens, this 
      interaction may represent an important target in the treatment of New World 
      hemorrhagic fevers. In addition, the ability to use TfR1 may be a useful tool to 
      predict the likelihood that any existing or newly discovered viruses in this 
      family could infect humans.
FAU - Flanagan, Meg L
AU  - Flanagan ML
AD  - Saban Research Institute of Childrens Hospital Los Angeles, Los Angeles, 
      California 90027, USA.
FAU - Oldenburg, Jill
AU  - Oldenburg J
FAU - Reignier, Therese
AU  - Reignier T
FAU - Holt, Nathalia
AU  - Holt N
FAU - Hamilton, Genevieve A
AU  - Hamilton GA
FAU - Martin, Vanessa K
AU  - Martin VK
FAU - Cannon, Paula M
AU  - Cannon PM
LA  - eng
GR  - U54 AI065359/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20071114
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (Antigens, CD)
RN  - 0 (CD71 antigen)
RN  - 0 (Glycoproteins)
RN  - 0 (Receptors, Transferrin)
RN  - 0 (Receptors, Virus)
RN  - 0 (Viral Proteins)
SB  - IM
MH  - Animals
MH  - Antigens, CD/*physiology
MH  - Arenaviruses, New World/*physiology
MH  - Cats
MH  - Cell Line
MH  - Dogs
MH  - Glycoproteins/*physiology
MH  - Humans
MH  - Mice
MH  - Receptors, Transferrin/*physiology
MH  - Receptors, Virus/*physiology
MH  - Viral Proteins/*physiology
MH  - *Virus Internalization
PMC - PMC2224602
EDAT- 2007/11/16 09:00
MHDA- 2008/01/25 09:00
PMCR- 2008/05/01
CRDT- 2007/11/16 09:00
PHST- 2007/11/16 09:00 [pubmed]
PHST- 2008/01/25 09:00 [medline]
PHST- 2007/11/16 09:00 [entrez]
PHST- 2008/05/01 00:00 [pmc-release]
AID - JVI.01397-07 [pii]
AID - 1397-07 [pii]
AID - 10.1128/JVI.01397-07 [doi]
PST - ppublish
SO  - J Virol. 2008 Jan;82(2):938-48. doi: 10.1128/JVI.01397-07. Epub 2007 Nov 14.