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The intracellular bacterium <i>Wolbachia</i> is increasingly being utilised in control programs to limit the spread of arboviruses by <i>Aedes</i> mosquitoes. Achieving a better understanding of how <i>Wolbachia</i> strains can reduce viral replication/spread could be important for the long-term success of such programs. Previous studies have indicated that for some strains of <i>Wolbachia</i>, perturbations in lipid metabolism and cholesterol storage are vital in <i>Wolbachia</i>-mediated antiviral activity against the flaviviruses dengue and Zika; however, it has not yet been examined whether arboviruses in the alphavirus group are affected in the same way. Here, using the reporters for the alphavirus Semliki Forest virus (SFV) in <i>Aedes albopictus</i> cells, we found that <i>Wolbachia</i> strains <i>w</i>Mel, <i>w</i>Au and <i>w</i>AlbB blocked viral replication/translation early in infection and that storage of cholesterol in lipid droplets is not key to this inhibition. Another alphavirus, o’nyong nyong virus (ONNV), was tested in both <i>Aedes albopictus</i> cells and in vivo in stable, transinfected <i>Aedes aegypti</i> mosquito lines. The strains <i>w</i>Mel, <i>w</i>Au and <i>w</i>AlbB show strong antiviral activity against ONNV both in vitro and in vivo. Again, 2-hydroxypropyl-β-cyclodextrin (2HPCD) was not able to rescue ONNV replication in cell lines, suggesting that the release of stored cholesterol caused by <i>w</i>Mel is not able to rescue blockage of ONNV. Taken together, this study shows that alphaviruses appear to be inhibited early in replication/translation and that there may be differences in how alphaviruses are inhibited by <i>Wolbachia</i> in comparison to flaviviruses.