75122 Federal Register / Vol. 73, No. 238 / Wednesday, December 10, 2008 / Notices 

Collaborative Research Opportunity: 

The NIAID, OTD, is seeking statements 

of capability or interest from parties 

interested in collaborative research to 

further develop, evaluate, or 

commercialize this ‘‘Discovery of Novel 

Pharmacophores Inhibiting the Growth 

of Mycobacterium Tuberculosis’’. Please 

contact Anna Amar at 301–451–3525 for 

more information. 

A Varicella-Zoster Virus Mutant That Is 

Markedly Impaired for Latent Infection 

Available for the Development of 

Shingles Vaccines and Diagnostics 

Description of Technology: 

Reactivation of latent Varicella-Zoster 

virus (VZV) infection is the cause of 

shingles, which is prominent in adults 

over the age of 60 and individuals who 

have compromised immune systems, 

due to HIV infection, cancer treatment 

and/or transplant. Shingles is a 

worldwide health concern that affects 

approximately 600,000 Americans each 

year. The incidence of shingles is also 

high in Europe, South America, and 

India; the latter having an estimated two 

million individuals affected, yearly. 

Recent research studies show that VZV 

vaccines have a significant effect on 

decreasing the incidence of shingles in 

elderly. 

The current technology describes 

compositions, cells and methods related 

to the production and use of a mutant 

VZV and the development of vaccines 

against the infectious agent. Latent VZV 

expresses a limited repertoire of viral 

genes including the following six open 

reading frames (ORFs): 4, 21, 29, 62, 63, 

and 66. The present invention describes 

an ORF29 mutant VZV that 

demonstrates a weakened ability to 

establish latency in animal studies. The 

current technology provides methods 

for using the mutant in the development 

of live vaccines and diagnostic tools. A 

related invention is described in PCT/ 

US05/021788 (publication number 

WO2006012092). 

Applications: Development of 

vaccines and diagnostics for prevention 

of shingles. 

Development Status: Pre-clinical 

studies have been performed to 

demonstrate the reduced latency of the 

ORF29 mutant VZV in animals. 

Inventors: Jeffrey Cohen (NIAID) and 

Lesley Pesnicak (NIAID). 

Patent Status: U.S. Provisional 

Application No. 60/857,766 filed 09 

Nov 2006 (HHS Reference No. E–029– 

2007/0–US–01); PCT Application No. 

PCT/US2007/084331 filed 09 Nov 2007, 

which published as WO 2008/079539 

on 03 Jul 2008 (HHS Reference No. E– 

029–2007/0–PCT–02). 

Licensing Status: Available for 

licensing and commercial development. 

Licensing Contact: Kevin W. Chang, 

Ph.D.; 301–435–5018; 

changke@mail.nih.gov. 

Collaborative Research Opportunity: 

The NIAID Laboratory of Clinical 

Infectious Diseases is seeking statements 

of capability or interest from parties 

interested in collaborative research to 

further develop, evaluate, or 

commercialize vaccine strains of VZV 

vaccine with impaired latency. Please 

contact Kelly Murphy, J.D., M.S., at 301/ 

451–3523 or murphykt@niaid.nih.gov 

for more information. 

Anti-Plasmodium Compositions and 

Methods of Use 

Description of Technology: The 

present invention comprises peptides/ 

antibodies specific for the binding 

proteins of Plasmodium, a parasite 

responsible for malaria, hence in effect 

blocking the parasite’s binding to the 

erythrocytes. Also included are methods 

for their use in preventing, diagnosing 

or treating the related infections. 

Although malaria is virtually 

eradicated in the United States, it 

continues to be one of the most serious 

infectious diseases in the world, killing 

millions of people each year in the 

countries throughout Africa, Asia and 

Latin America. In fact, over 41% of the 

world population lives in the regions 

affected by malaria. In vitro studies 

using the antibodies described in the 

current technology showed ∼80% 

reduction in the number of blood cells 

infected with Plasmodium parasite. 

Infectivity studies using peptides 

demonstrated that they are also 

specifically able to prevent binding of 

parasites to blood cells. The claimed 

antibodies and peptides can also be 

used for immunization of humans and 

animals, or for development of 

diagnostic kits capable of detecting the 

presence, localization and quantity of 

the Plasmodium parasites in tissues and 

cells. 

Applications: Diagnostics 

development; Vaccines development. 

Inventors: David L. Narum and Kim 

Lee Sim (NIAID). 

Relevant Publications: 

1. Sim BK, Narum DL, Liang H, 

Fuhrmann SR, Obaldia N 3rd, 

Gramzinski R, Aguiar J, Haynes JD, 

Moch JK, Hoffman SL. Induction of 

biologically active antibodies in mice, 

rabbits, and monkeys by Plasmodium 

falciparum EBA–175 region II DNA 

vaccine. Mol Med. 2001 Apr;7(4):247– 

254. 

2. Narum DL, Haynes JD, Fuhrmann 

S, Moch K, Liang H, Hoffman SL, Sim 

BK. Antibodies against the Plasmodium 

falciparum receptor binding domain of 

EBA–175 block invasion pathways that 

do not involve sialic acids. Infect 

Immun. 2000 Apr;68(4):1964–1966. 

3. Liang H, Narum DL, Fuhrmann SR, 

Luu T, Sim BK. A recombinant 

baculovirus-expressed Plasmodium 

falciparum receptor-binding domain of 

erythrocyte binding protein EBA–175 

biologically mimics native protein. 

Infect Immun. 2000 Jun;68(6):3564– 

3568. 

Patent Status: HHS Reference No. E– 

004–2004/2— 

• U.S. Patent No. 7,025,961 issued 11 

Apr 2006 

• Australian Patent No. 20042011615 

issued 11 May 2007 

• Canadian Application No. 

CA236247 

• Japanese Application No. JP2000– 

602280 (published as JP,2002– 

540770,A) 

Licensing Status: Available for 

exclusive or non-exclusive licensing. 

Licensing Contact: RC Tang, JD, LLM; 

301–435–5031; tangr@mail.nih.gov 

Dated: December 1, 2008. 

Richard U. Rodriguez, 

Director, Division of Technology Development 

and Transfer, Office of Technology Transfer, 

National Institutes of Health. 

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Correction 

In notice document E8–26726 

beginning on page 71858 in the issue 

ofTuesday, November 25, 2008, make 

the following correction: 

On page 71858, in the first column, 

under the DATES heading, in the first 

line, ‘‘Effective Date: March 25, 2008’’ 

shouldread ‘‘Effective Date: May 1, 

2010’’. 

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