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Port Meadow flooded, February 2021

Professor Richard Berry D. Phil.

Professor of Biological Physics

Research theme

  • Biological physics

Sub department

  • Condensed Matter Physics

Research groups

  • Oxford Molecular Motors
Richard.Berry@physics.ox.ac.uk
Telephone: 01865 (2)72288,01865 (2)71723
Clarendon Laboratory, room 273B
  • About
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The bacterial flagella motor

ADVANCES IN MICROBIAL PHYSIOLOGY, VOL 41 41 (1999) 291-337

Authors:

RM Berry, JP Armitage

Absence of a barrier to backwards rotation of the bacterial flagellar motor demonstrated with optical tweezers

Proceedings of the National Academy of Sciences of the United States of America Proceedings of the National Academy of Sciences 94:26 (1997) 14433-14437

Authors:

Richard M Berry, Howard C Berg

Torque generated by the bacterial flagellar motor close to stall

Biophysical Journal Elsevier 71:6 (1996) 3501-3510

Authors:

RM Berry, HC Berg

Mechanical limits of bacterial flagellar motors probed by electrorotation

Biophysical Journal Elsevier 69:1 (1995) 280-286

Authors:

RM Berry, L Turner, HC Berg

Defective escape mutants of HIV.

J Theor Biol 171:4 (1994) 387-395

Authors:

RM Berry, MA Nowak

Abstract:

The virological literature presents two broad types of defective virus mutants that can alter the outcome of viral infection. In some infections, defective interfering particles reduce the replication of wild-type virus and lead to an attenuated or persistent infection. In other cases, very specific and highly pathogenic defective mutants lead to virulent disease in the presence of a much less pathogenic but replication-competent helper virus. Here, we outline the theoretical possibility that defective mutants of HIV, which escape from some of the immune responses directed at the wild-type virus, can have a positive effect on total virus growth in HIV infections. The high error rate of HIV may generate many mutants that have some altered epitope (escape mutants), but at the cost of greatly reduced or completely impaired reproductive abilities. If these mutants retain some ability to impair immune cell function, then the production of such "defective escape" mutants may enhance overall virus reproduction. This will be illustrated by a mathematical model.

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