PMID- 7576319
OWN - NLM
STAT- MEDLINE
DCOM- 19951220
LR  - 20190718
IS  - 0269-9370 (Print)
IS  - 0269-9370 (Linking)
VI  - 9
IP  - 8
DP  - 1995 Aug
TI  - Productive HIV-1 infection of normal human mammary epithelial cells.
PG  - 859-66
AB  - OBJECTIVE AND DESIGN: To determine the susceptibility of mammary epithelial cells 
      (MEC) to HIV-1 as breastfeeding is an established route of HIV transmission, 
      although the origin of virus in breastmilk is unclear. METHODS: Primary 
      epithelial cell cultures were derived from the mammary glands of healthy donors; 
      immortalized MEC lines were also used. HIV infection was followed by detection of 
      infectious particle production, p24 antigen and viral sequences. RESULTS: Seven 
      out of 11 primary MEC cultures and two out of three MEC lines were productively 
      infected by HIV-1. Virus replication significantly reduced cell proliferation, 
      although cell viability was only slightly affected. Cytopathic changes were not 
      observed. MEC cultures expressed low levels of surface CD4, galactosylceramide 
      and CD26, but essentially no human leukocyte antigen (HLA)-DR. Infection of 
      HIV-permissive MEC cells was associated with the upregulation of surface HLA-DR 
      and CD26. In contrast, the expression of CD4, tissue-specific markers, adhesion 
      molecules and growth-factor receptors was downregulated. To a lesser extent, 
      similar effects were also observed in non-permissive cells. Hormones 
      (triiodothyronine plus beta-estradiol and prolactin) enhanced HIV replication, 
      possibly through the stimulation of cellular DNA synthesis. CONCLUSIONS: We 
      concluded that HIV-1 replication in ductal/alveolar MEC may be, in part, 
      responsible for the presence of HIV-1 in milk; that hormones may stimulate virus 
      replication; and that infection reduces the growth of epithelial cells. Although 
      in vitro HIV is produced by MEC to a lesser extent than lymphoid cells, 
      MEC-derived HIV might have selective advantages for the infection of mucosal 
      epithelial cells during breastfeeding.
FAU - Toniolo, A
AU  - Toniolo A
AD  - Institute of Medicine and Public Health, University of Pavia, Varese, Italy.
FAU - Serra, C
AU  - Serra C
FAU - Conaldi, P G
AU  - Conaldi PG
FAU - Basolo, F
AU  - Basolo F
FAU - Falcone, V
AU  - Falcone V
FAU - Dolei, A
AU  - Dolei A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - AIDS
JT  - AIDS (London, England)
JID - 8710219
RN  - 0 (Hormones)
SB  - IM
MH  - Breast/cytology/*virology
MH  - Breast Feeding
MH  - Cell Line
MH  - Epithelial Cells
MH  - Epithelium/virology
MH  - Female
MH  - HIV Infections/*etiology/transmission/virology
MH  - *HIV-1/pathogenicity/physiology
MH  - Hormones/pharmacology
MH  - Humans
MH  - Infant, Newborn
MH  - Infectious Disease Transmission, Vertical
MH  - Milk, Human/virology
MH  - Phenotype
MH  - Pregnancy
MH  - Virus Replication
EDAT- 1995/08/01 00:00
MHDA- 1995/08/01 00:01
CRDT- 1995/08/01 00:00
PHST- 1995/08/01 00:00 [pubmed]
PHST- 1995/08/01 00:01 [medline]
PHST- 1995/08/01 00:00 [entrez]
AID - 10.1097/00002030-199508000-00005 [doi]
PST - ppublish
SO  - AIDS. 1995 Aug;9(8):859-66. doi: 10.1097/00002030-199508000-00005.