#PAGE_PARAMS# #ADS_HEAD_SCRIPTS# #MICRODATA#

Distinct Patterns of IFITM-Mediated Restriction of Filoviruses, SARS Coronavirus, and Influenza A Virus


Interferon-inducible transmembrane proteins 1, 2, and 3 (IFITM1, 2, and 3) are recently identified viral restriction factors that inhibit infection mediated by the influenza A virus (IAV) hemagglutinin (HA) protein. Here we show that IFITM proteins restricted infection mediated by the entry glycoproteins (GP1,2) of Marburg and Ebola filoviruses (MARV, EBOV). Consistent with these observations, interferon-β specifically restricted filovirus and IAV entry processes. IFITM proteins also inhibited replication of infectious MARV and EBOV. We observed distinct patterns of IFITM-mediated restriction: compared with IAV, the entry processes of MARV and EBOV were less restricted by IFITM3, but more restricted by IFITM1. Moreover, murine Ifitm5 and 6 did not restrict IAV, but efficiently inhibited filovirus entry. We further demonstrate that replication of infectious SARS coronavirus (SARS-CoV) and entry mediated by the SARS-CoV spike (S) protein are restricted by IFITM proteins. The profile of IFITM-mediated restriction of SARS-CoV was more similar to that of filoviruses than to IAV. Trypsin treatment of receptor-associated SARS-CoV pseudovirions, which bypasses their dependence on lysosomal cathepsin L, also bypassed IFITM-mediated restriction. However, IFITM proteins did not reduce cellular cathepsin activity or limit access of virions to acidic intracellular compartments. Our data indicate that IFITM-mediated restriction is localized to a late stage in the endocytic pathway. They further show that IFITM proteins differentially restrict the entry of a broad range of enveloped viruses, and modulate cellular tropism independently of viral receptor expression.


Vyšlo v časopise: Distinct Patterns of IFITM-Mediated Restriction of Filoviruses, SARS Coronavirus, and Influenza A Virus. PLoS Pathog 7(1): e32767. doi:10.1371/journal.ppat.1001258
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1001258

Souhrn

Interferon-inducible transmembrane proteins 1, 2, and 3 (IFITM1, 2, and 3) are recently identified viral restriction factors that inhibit infection mediated by the influenza A virus (IAV) hemagglutinin (HA) protein. Here we show that IFITM proteins restricted infection mediated by the entry glycoproteins (GP1,2) of Marburg and Ebola filoviruses (MARV, EBOV). Consistent with these observations, interferon-β specifically restricted filovirus and IAV entry processes. IFITM proteins also inhibited replication of infectious MARV and EBOV. We observed distinct patterns of IFITM-mediated restriction: compared with IAV, the entry processes of MARV and EBOV were less restricted by IFITM3, but more restricted by IFITM1. Moreover, murine Ifitm5 and 6 did not restrict IAV, but efficiently inhibited filovirus entry. We further demonstrate that replication of infectious SARS coronavirus (SARS-CoV) and entry mediated by the SARS-CoV spike (S) protein are restricted by IFITM proteins. The profile of IFITM-mediated restriction of SARS-CoV was more similar to that of filoviruses than to IAV. Trypsin treatment of receptor-associated SARS-CoV pseudovirions, which bypasses their dependence on lysosomal cathepsin L, also bypassed IFITM-mediated restriction. However, IFITM proteins did not reduce cellular cathepsin activity or limit access of virions to acidic intracellular compartments. Our data indicate that IFITM-mediated restriction is localized to a late stage in the endocytic pathway. They further show that IFITM proteins differentially restrict the entry of a broad range of enveloped viruses, and modulate cellular tropism independently of viral receptor expression.


Zdroje

1. BrassAL

HuangIC

BenitaY

JohnSP

KrishnanMN

2009 The IFITM proteins mediate cellular resistance to influenza A H1N1 virus, West Nile virus, and dengue virus. Cell 139 1243 1254

2. FriedmanRL

ManlySP

McMahonM

KerrIM

StarkGR

1984 Transcriptional and posttranscriptional regulation of interferon-induced gene expression in human cells. Cell 38 745 755

3. MoffattP

GaumondMH

SaloisP

SellinK

BessetteMC

2008 Bril: a novel bone-specific modulator of mineralization. J Bone Miner Res 23 1497 1508

4. LangeUC

SaitouM

WesternPS

BartonSC

SuraniMA

2003 The fragilis interferon-inducible gene family of transmembrane proteins is associated with germ cell specification in mice. BMC Dev Biol 3 1

5. TanakaSS

YamaguchiYL

TsoiB

LickertH

TamPP

2005 IFITM/Mil/fragilis family proteins IFITM1 and IFITM3 play distinct roles in mouse primordial germ cell homing and repulsion. Dev Cell 9 745 756

6. HarrisonSC

2008 Viral membrane fusion. Nat Struct Mol Biol 15 690 698

7. SkehelJJ

WileyDC

2000 Receptor binding and membrane fusion in virus entry: the influenza hemagglutinin. Annu Rev Biochem 69 531 569

8. StiasnyK

HeinzFX

2006 Flavivirus membrane fusion. J Gen Virol 87 2755 2766

9. MiyauchiK

KimY

LatinovicO

MorozovV

MelikyanGB

2009 HIV enters cells via endocytosis and dynamin-dependent fusion with endosomes. Cell 137 433 444

10. HuangIC

BoschBJ

LiF

LiW

LeeKH

2006 SARS coronavirus, but not human coronavirus NL63, utilizes cathepsin L to infect ACE2-expressing cells. J Biol Chem 281 3198 3203

11. SimmonsG

GosaliaDN

RennekampAJ

ReevesJD

DiamondSL

2005 Inhibitors of cathepsin L prevent severe acute respiratory syndrome coronavirus entry. Proc Natl Acad Sci U S A 102 11876 11881

12. ChandranK

SullivanNJ

FelborU

WhelanSP

CunninghamJM

2005 Endosomal proteolysis of the Ebola virus glycoprotein is necessary for infection. Science 308 1643 1645

13. SchornbergK

MatsuyamaS

KabschK

DelosS

BoutonA

2006 Role of endosomal cathepsins in entry mediated by the Ebola virus glycoprotein. J Virol 80 4174 4178

14. WongAC

SandesaraRG

MulherkarN

WhelanSP

ChandranK

A forward genetic strategy reveals destabilizing mutations in the Ebolavirus glycoprotein that alter its protease dependence during cell entry. J Virol 84 163 175

15. BelouzardS

ChuVC

WhittakerGR

2009 Activation of the SARS coronavirus spike protein via sequential proteolytic cleavage at two distinct sites. Proc Natl Acad Sci U S A 106 5871 5876

16. MatsuyamaS

UjikeM

MorikawaS

TashiroM

TaguchiF

2005 Protease-mediated enhancement of severe acute respiratory syndrome coronavirus infection. Proc Natl Acad Sci U S A 102 12543 12547

17. TurkV

TurkB

TurkD

2001 Lysosomal cysteine proteases: facts and opportunities. Embo J 20 4629 4633

18. HuangIC

LiW

SuiJ

MarascoW

ChoeH

2008 Influenza A virus neuraminidase limits viral superinfection. J Virol 82 4834 4843

19. RadoshitzkySR

AbrahamJ

SpiropoulouCF

KuhnJH

NguyenD

2007 Transferrin receptor 1 is a cellular receptor for New World haemorrhagic fever arenaviruses. Nature 446 92 96

20. KuhnJH

RadoshitzkySR

GuthAC

WarfieldKL

LiW

2006 Conserved receptor-binding domains of Lake Victoria marburgvirus and Zaire ebolavirus bind a common receptor. J Biol Chem 281 15951 15958

21. LiW

MooreMJ

VasilievaN

SuiJ

WongSK

2003 Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus. Nature 426 450 454

22. ChenC

ZhuangX

2008 Epsin 1 is a cargo-specific adaptor for the clathrin-mediated endocytosis of the influenza virus. Proc Natl Acad Sci U S A 105 11790 11795

23. BieniaszPD

2004 Intrinsic immunity: a front-line defense against viral attack. Nat Immunol 5 1109 1115

24. MpanjuOM

TownerJS

DoverJE

NicholST

WilsonCA

2006 Identification of two amino acid residues on Ebola virus glycoprotein 1 critical for cell entry. Virus Res 121 205 214

25. BeckerMM

GrahamRL

DonaldsonEF

RockxB

SimsAC

2008 Synthetic recombinant bat SARS-like coronavirus is infectious in cultured cells and in mice. Proc Natl Acad Sci U S A 105 19944 19949

26. WongSK

LiW

MooreMJ

ChoeH

FarzanM

2004 A 193-amino acid fragment of the SARS coronavirus S protein efficiently binds angiotensin-converting enzyme 2. J Biol Chem 279 3197 3201

Štítky
Hygiena a epidemiológia Infekčné lekárstvo Laboratórium

Článok vyšiel v časopise

PLOS Pathogens


2011 Číslo 1
Najčítanejšie tento týždeň
Najčítanejšie v tomto čísle
Kurzy

Zvýšte si kvalifikáciu online z pohodlia domova

Aktuální možnosti diagnostiky a léčby litiáz
nový kurz
Autori: MUDr. Tomáš Ürge, PhD.

Všetky kurzy
Prihlásenie
Zabudnuté heslo

Zadajte e-mailovú adresu, s ktorou ste vytvárali účet. Budú Vám na ňu zasielané informácie k nastaveniu nového hesla.

Prihlásenie

Nemáte účet?  Registrujte sa

#ADS_BOTTOM_SCRIPTS#