Biology Reference
In-Depth Information
tion is likely to be useful for assessing phenotypic changes that occur in cells
from infected persons.
CONCLUSION
The investigation of HIV-1 infection and disease pathogenesis has been sig-
ni®cantly a¨ected by the capacity to analyze single cells by ¯ow cytometry. The
technology provides for fast and e½cient analysis of large numbers of cells,
measuring for multiple parameters simultaneously. Moreover, the capability of
sorting selected populations based on the analysis on a ¯ow cytometer adds
a signi®cant dimension to the potential for investigating the consequences of
HIV-1 infection in vivo and in vitro.
Nevertheless, ¯ow cytometric analysis has been hampered by a major limi-
tation: the poor sensitivity of the analysis compared with other techniques.
Most importantly, many molecules are expressed in functionally signi®cant
amounts that cannot be detected by the most sensitive current ¯ow cytometric
methods.
Enzymatic ampli®cation technology allows for a 100-fold enhancement of
the ¯uorescent signal and, consequently, the expression of molecules that could
not be detected by standard procedures can now be observed. To be able to
track the expression levels of functionally signi®cant molecules on a cell-by-cell
basis in an e½cient and timely manner represents a major improvement in the
technical capabilities for investigators working to understand the pathogenesis
of HIV-1 disease.
REFERENCES
Aiken C, Konner J, Landau NR, Lenburg ME, Trono D. 1994. Nef induces CD4 endocytosis: re-
quirement for a critical dileucine motif in the membrane-proximal CD4 cytoplasmic domain.
Cell 76: 853±864.
Akridge RE, Oyafuso LKM, Reed SG. 1994. IL-10 is induced during HIV-1 infection and is capa-
ble of decreasing viral replication in human macrophages. J Immunol 153: 5782±5789.
Alsmadi O, Herz R, Murphy E, Pinter A, Tilley SA. 1997. A novel antibody-dependent cellular
cytotoxicity epitope in gp120 is identi®ed by two monoclonal antibodies isolated from a long-
term survivor of human immunode®ciency virus type 1 infection. J Virol 71: 925±933.
Appay V, Nixon DF, Donahoe SM, Gillespie GMA, Dong T, King A, Ogg GS, Spiegel HML,
Conlon C, Spina CA, Havlir DV, Richman DD, Waters A, Easterbrook P, McMichael AJ,
Rowland-Jones SL. 2000. HIV-speci®c CD8 T cells produce antiviral cytokines but are im-
paired in cytolytic function. J Exp Med 192: 63±75.
Arenzana-Seisdedos F, Virelizier J, Rousset D, Clark-Lewis I, Loetscher P, Moser B, Baggiolini M.
1996. HIV blocked by chemokine antagonist. Nature 383: 400.
Ayyavoo V, Mahboubi A, Mahalingam S, Ramalingam R, Kudchodkar S, Williams WV, Green
DR, Weiner DB. 1997. HIV-1 Vpr suppresses immune activation and apoptosis through regu-
lation of nuclear factor kB. Nature Med 3: 1117±1123.
Search WWH ::




Custom Search